Six years of aerial and ground monitoring surveys for sudden oak death in California

Treesearch

Lisa Bell; Jeff Mai; Zachary Heath; Erik Haunreiter; Lisa M. Fischer

2008-01-01

Aerial surveys have been conducted since 2001 to map recent hardwood mortality and consequently target ground visits for detection of Phytophthora ramorum, the pathogen that causes sudden oak death (SOD). Each year the aerial and ground surveys monitored much of California?s forests at risk for SOD resulting in new maps of hardwood mortality,...

Effects of Sudden Oak Death on the crown fire ignition potential of tanoak (Lithocarpus densiflorus)

Treesearch

Howard Kuljian; J. Morgan Varner

2010-01-01

In the face of the sudden oak death (SOD) epidemic, decreasing foliar moisture content (FMC) of tanoak (Lithocarpus densiflorus) has land managers, fire managers, and property owners concerned with the increased possibility of crown fire in affected areas. A need exists to link local SOD-affected foliar moisture content (FMC) values and current FMC...

Novel interactions between wildfire and sudden oak death influence sexual and asexual regeneration in coast redwood forests

Treesearch

Allison B. Simler; Margaret R. Metz; Ross K. Meentemeyer; Kerri M. Frangioso; David M. Rizzo

2017-01-01

Novel interactions between compounded disturbances can leave lasting ecological legacies on communities and alter regeneration trajectories. Sudden oak death (SOD), caused by Phytophthora ramorum, is a biotic disturbance, an emerging disease causing widespread oak and tanoak mortality in California’s coastal forests....

Managing redwood ecosystems using Sudden Oak Death as a silvicultural tool

Treesearch

Frederick D. Euphrat

2015-01-01

In response to the wave of sudden oak death (SOD), caused by Phytophthora ramorum, sweeping the redwood forest ecosystems of California's North Coast, the role of foresters and other ecosystem managers is being tested. On Bear Flat Tree Farm, near Healdsburg, California, Forest, Soil & Water, Inc. (FSW) has conducted a multi-year,...

Conditions 10 years after sudden oak death suppression treatments in Humboldt County, California

Treesearch

Yana Valachovic; Richard Cobb; Brendan Twieg

2017-01-01

In 2006, three isolated sudden oak death- (SOD) infested locations within Humboldt County were selected for silvicultural treatments that targeted the removal and/or reduction of tanoak (Notholithocarpus densiflorus Hook. & Arn.) and California bay laurel (Umbellularia californica Hook. & Arn), the main hosts...

Multi-scale data to assess and monitor sudden oak death

Treesearch

Lisa M. Levien; Chris S. Fischer; Lianne C. Mahon; Jeff A. Mai

2002-01-01

The USDA Forest Service (FS) and California Department of Forestry and Fire Protection (CDF) are monitoring Sudden Oak Death (SOD) under the umbrella of the larger California Land Cover Mapping and Monitoring Program (LCMMP). The LCMMP is a statewide cooperative effort among the FS and CDF focused on mapping and monitoring California’s vegetation and land cover.

Understanding sudden oak death: a model of partnership and collaboration

Treesearch

Jimmy L. Reaves

2006-01-01

Good morning. I want to thank the planning committee for allowing me to share some of my thoughts at this Symposium as we try to better understand sudden oak death (SOD) and Phytophthora ramorum. I bring you regards from Dr. Ann Bartuska, the Deputy Chief for Forest Service Research and Development. Ann is a big supporter of the work that has already...

Intraspecific variation in host susceptibility and climatic factors mediate epidemics of sudden oak death in western US forests

Treesearch

D. Huberli; K.J. Hayden; M. Calver; M. Garbelotto

2011-01-01

Umbellularia californica is one of the key infectious hosts of the exotic Phytophthora ramorum, which causes sudden oak death (SOD) in California and Oregon forests. This study provides a comprehensive analysis of the epidemiologically relevant parameters for SOD in California and southern Oregon, including potential differences between the two...

Development of a management plan for coast live oak forests affected by sudden oak death in East Bay Regional Parks

Treesearch

Brice A. McPherson; Joshua O’Neill; Gregory Biging; Maggi Kelly; David L. Wood

2015-01-01

The East Bay Regional Park District maintains the largest urban park system in the United States, comprising over 45 000 ha, and more than 1900 km of trails, with extensive forests bordering residential areas. Sudden oak death (SOD), caused by the introduced oomycete Phytophthora ramorum, was first detected in a district park in 2001. Both...

Sudden Oak Death in redwood forests: vegetation dynamics in the wake of tanoak decline

Treesearch

Benjamin Ramage; Kevin O’Hara

2010-01-01

Numerous lines of inquiry have concluded that tanoak (Lithocarpus densiflorus) will continue to experience drastic population declines and may even disappear entirely from redwood (Sequoia sempervirens) forests as a result of the exotic disease sudden oak death (SOD) (Maloney and others 2005, McPherson and others 2005,...

Phytophthora ramorum and sudden oak death in California: IV. preliminary studies on chemical control

Treesearch

Matteo Garbelotto; David M. Rizzo; Lawrence Marais

2002-01-01

Chemical applications may provide one means of control for Phytophthora ramorum, the cause of Sudden Oak Death (SOD). Such controls have been effective with other Phytophthora species in landscape and orchard situations. We have initiated laboratory and field studies to test the efficacy of a number of products previously reported...

USDA Forest Service, Pacific Southwest Research Station Sudden Oak Death Research Program: 2001-2005

Treesearch

Patrick J. Shea

2006-01-01

The Pacific Southwest Research Station (PSW), U.S. Department of Agriculture (USDA) Forest Service initiated the Sudden Oak Death Research (SOD) Program in late 2000. The program was prompted by late fiscal year funding dedicated directly to begin research on this newly discovered disease. The history of discovery of Phytophthora ramorum, the...

Phytophthora ramorum and sudden oak death in California: III. preliminary studies in pathogen genetics

Treesearch

Matteo Garbelotto; David M. Rizzo; Katie Hayden; Monica Meija-Chang; Jennifer M. Davidson; Steven Tjosvold

2002-01-01

Sudden oak death (SOD) has been shown to be caused by a new species of Phytophthora, P. ramorum. A basic understanding of the genetics of P. ramorum is critical to any management strategy. We have initiated a number of studies to examine species concepts, population biology and mating behavior of the pathogen....

Fire behavioral changes as a result of sudden oak death in coastal California forests

Treesearch

Y. Vlachovic; C. Lee; H. Scanlon; J.M. Varner; R. Glebocki; B.D. Graham; D.M. Rizzo

2013-01-01

Field observations and anecdotal evidence suggest that sudden oak death (SOD), a disease caused by the pathogen Phytophthora ramorum, may alter fuel loading in affected forests. Though it is reasonable to assume that a disease resulting in leaf blight, dead branches, and tree mortality would increase forest fuels, little work has been done to...

Phenotypic diversification is associated with host-induced transposon derepression in the sudden oak death pathogen Phytophthora ramorum

Treesearch

T. Kasuga; M. Kozanitas; M. Bui; D. Huberli; D. M. Rizzo; M. Garbelotto

2012-01-01

The oomycete pathogen Phytophthora ramorum is responsible for sudden oak death (SOD) in California coastal forests. P. ramorum is a generalist pathogen with over 100 known host species. Three or four closely related genotypes of P. ramorum (from a single lineage) were...

Aerial application of Agri-Fos® to prevent Sudden Oak Death in Oregon tanoak forests

Treesearch

Alan Kanaskie; Everett Hansen; Wendy Sutton; Paul Reeser; Carolyn Choquette

2010-01-01

We have been testing the practicality and efficacy of aerial application of Agri-Fos® for control of sudden oak death (SOD) in the Oregon tanoak (Lithocarpus densiflorus) forest. Helicopter application to forest stands has been compared with bole injection and groundbased spray application to seedlings and stump sprouts. We bio-assayed...

Sudden Oak Death - Western (Pest Alert)

Treesearch

Susan Frankel

2002-01-01

Tens of thousands of tanoak (Lithocarpus densiflorus), coast live oak (Quercus agrifolia), California black oak (Quercus kelloggii), Shreve oak (Quercus parvula var. shrevei), and madrone (Arbutus menziesii) have been killed by a newly identified species, Phytophthora ramorum, which causes Sudden Oak Death. Sudden Oak Death was first reported in 1995 in central coastal...

Mapping the risk of sudden oak death in Oregon: prioritizing locations for early detection and eradication

Treesearch

V& aacute; clavík Tom& aacute; & scaron; ; Alan Kanaskie; Ellen Goheen; Janet Ohmann; Everett Hansen; Ross Meentemeyer

2010-01-01

Phytophthora ramorum was first discovered in forests of southwestern Oregon in 2001. Despite intense eradication efforts, disease continues to spread from initially infested sites because of the late discovery of disease outbreaks and incomplete detection. Here we present two GIS predictive models of sudden oak death (SOD) establishment and spread...

Temporal fluctuations and the role of disturbance in disease progression of the sudden oak death epidemic

Treesearch

Melina Kozanitas; Todd W. Osmundson; Matteo Garbelotto

2013-01-01

With its high host mortality and ability to cause landscape-scale alterations in forest cover and composition, sudden oak death (SOD) (etiological agent Phytophthora ramorum, Stramenopila, Oomycota) mirrors past forest disease epidemics such as Chestnut Blight and Dutch Elm Disease. In contrast with these past epidemics, however, the appearance of...

Etiology and evidence of systemic acidification in SOD-affected forests of California

Treesearch

Lee Klinger; Ralph Zingaro

2006-01-01

Pathologists investigating the widespread death of oak trees in the forest ecosystems of northern California concluded, in 2000, that the problem was due to a new plant disease, dubbed sudden oak death (SOD), which is caused by the fungal pathogen Phytophthora ramorum. Since then this one organism has been the focal point of notable efforts to...

Lessons learned from the USDA Forest Service, Pacific Southwest Region, sudden oak death management program

Treesearch

Phil Cannon; Susan J. Frankel; Pete Angwin

2017-01-01

Over the past 15 years, the USDA Forest Service, Pacific Southwest Region, State and Private Forestry (S&PF) has provided grants which have supported over 200 projects to address sudden oak death (SOD) in California. To date, over $10 million has been provided by US taxpayers, plus an additional $8 million of non-federal matching funds. These funds...

The effects of sudden oak death on foliar moisture content and crown fire potential in tanoak

Treesearch

H. Kuljian; J.M. Varner

2010-01-01

The introduction of non-native pathogens can have profound effects on forest ecosystems resulting in loss of species, changes in species composition, and altered fuel structure. The introduction of Phytophthora ramorum, the pathogen recognized as causing Sudden Oak Death (SOD), leads to rapid decline and mortality of tanoak (Lithocarpus densiflorus) in forests of...

Sudden oak death disease progression in oaks and tanoaks

Treesearch

Brice A. McPherson; Sylvia R. Mori; David L. Wood; Andrew J. Storer; Pavel Svihra; N. Maggi Kelly; Richard B. Standiford

2006-01-01

In March 2000, we established twenty disease progression plots in Marin County to monitor the progress of sudden oak death symptoms in coast live oak (Quercus agrifolia), California black oak (Q. kelloggii), and tanoak (Lithocarpus densiflorus) (McPherson and others 2005). Plots were located to encompass a...

The effects of sudden oak death and wildfire on forest composition and dynamics in the Big Sur Ecoregion of Coastal California

Treesearch

Margaret R. Metz; Kerri M. Frangioso; Ross K. Meentemeyer; David M. Rizzo

2012-01-01

Sudden oak death (SOD), caused by Phytophthora ramorum, is an emerging forest disease associated with extensive tree mortality in coastal California forests (Rizzo et al. 2005). P. ramorum is a generalist pathogen that infects many hosts, but hosts differ in their ability to transmit the disease...

SOD-induced changes in foraging and nesting behavior of insectivorous, cavity-nesting birds

Treesearch

Kyle Apigian; Barbara Allen-Diaz

2006-01-01

Sudden oak death (SOD) is a tree disease caused by a recently described pathogen, Phytophthora ramorum. The disease affects dozens of plant species, but its effects are particularly pronounced in stands of coast live oak (Quercus agrifolia), often resulting in large stands with dead canopies and many downed trees. Such disease-...

Proceedings of the Sudden Oak Death Fourth Science Symposium

Treesearch

Susan J. Frankel; John T. Kliejunas; Katharine M. Palmieri

2010-01-01

The Sudden Oak Death Fourth Science Symposium provided a forum for current research on sudden oak death, caused by the exotic, quarantine pathogen, Phytophthora ramorum. Ninety submissions describing papers or posters on the following sudden oak death/P. ramorum topics are included: biology, genetics, nursery and wildland...

Proceedings of the sudden oak death third science symposium

Treesearch

Susan J. Frankel; John T. Kliejunas; Katharine M. Palmieri

2008-01-01

The Sudden Oak Death Third Science Symposium provided a forum for current research on sudden oak death, caused by the exotic, quarantine pathogen, Phytophthora ramorum. One hundred and seventeen submissions describing papers and posters on the following sudden oak death/ P. ramorum topics are included: biology, genetics, nursery,...

Proceedings of the sudden oak death sixth science symposium

Treesearch

Susan J. Frankel; Katharine M. Harrell

2017-01-01

The Sudden Oak Death Sixth Science Symposium provided a forum for current research on sudden oak death, caused by the exotic quarantine pathogen Phytophthora ramorum. More than 50 submissions describing papers or posters on the following sudden oak death/P. ramorum topics are included: biology, genetics, nursery and wildland...

Predicting the economic costs and property value losses attributed to sudden oak death damage in California (2010-2020).

PubMed

Kovacs, Kent; Václavík, Tomáš; Haight, Robert G; Pang, Arwin; Cunniffe, Nik J; Gilligan, Christopher A; Meentemeyer, Ross K

2011-04-01

Phytophthora ramorum, cause of sudden oak death, is a quarantined, non-native, invasive forest pathogen resulting in substantial mortality in coastal live oak (Quercus agrifolia) and several other related tree species on the Pacific Coast of the United States. We estimate the discounted cost of oak treatment, removal, and replacement on developed land in California communities using simulations of P. ramorum spread and infection risk over the next decade (2010-2020). An estimated 734 thousand oak trees occur on developed land in communities in the analysis area. The simulations predict an expanding sudden oak death (SOD) infestation that will likely encompass most of northwestern California and warrant treatment, removal, and replacement of more than 10 thousand oak trees with discounted cost of $7.5 million. In addition, we estimate the discounted property losses to single family homes of $135 million. Expanding the land base to include developed land outside as well as inside communities doubles the estimates of the number of oak trees killed and the associated costs and losses. The predicted costs and property value losses are substantial, but many of the damages in urban areas (e.g. potential losses from increased fire and safety risks of the dead trees and the loss of ecosystem service values) are not included. Copyright © 2010 Elsevier Ltd. All rights reserved.

Sudden Oak Death - Eastern (Pest Alert)

Treesearch

Joseph O' Brien; Manfred Mielke; Steve Oak; Bruce Moltzan

2002-01-01

A phenomenon known as Sudden Oak Death was first reported in 1995 in central coastal California. Since then, tens of thousands of tanoaks (Lithocarpus densiflorus), coast live oaks (Quercus agrifolia), and California black oaks (Quercus kelloggii) have been killed by a newly identified fungus, Phytophthora ramorum. On these hosts, the fungus causes a bleeding canker on...

Diagnosis and Management of Phytophthora ramorum canker in canyon live oak, an atypical bole canker host

Treesearch

Tedmund J. Swiecki; Elizabeth Bernhardt; Kamyar Aram; David Rizzo

2013-01-01

Diagnosis of sudden oak death (SOD) in tanoak (Notholithocarpus densiflorus (Hook. & Arn.) Manos, Cannon & S.H. Oh) and susceptible red/black oak species (coast live oak, Quercus agrifolia Née; Shreve oak, Q. parvula Greene var. shrevei (C.H. Mull.) Nixon; California...

Protecting Trees from Sudden Oak Death before Infection

Treesearch

C. Lee; Y. Valachovic; M. Garbelotto

2010-01-01

Phytophthora ramorum, an introduced invasive plant pathogen that causes sudden oak death, has killed over a million tanoak, coast live oak, Shreve oak, and California black oak trees along the California coastal region from Monterey through Humboldt Counties. Most trees infected with P. ramorum will eventually die, including...

Novel approaches to SOD management in California wildlands: a case study of "eradication" and collaboration in Redwood Valley

Treesearch

Y. Valachovic; L. Quinn-Davidson; E. Goldsworthy; P. Cannon

2013-01-01

In California, sudden oak death (SOD) treatment efforts have been localized, often targeting specific trees or properties. The widespread nature of SOD establishment and spread in coastal mountains of California has mostly precluded use of broader eradication strategies, which are more applicable in isolated infestations like those in Oregon. However, the 2010...

Welcome to the sudden oak death third science symposium

Treesearch

Susan J. Frankel

2008-01-01

On behalf of the United States Department of Agriculture (USDA)-Forest Service, Pacific Southwest Research Station and the California Oak Mortality Task Force, it is my pleasure to welcome you to the Sudden Oak Death Third Science Symposium. Looking back at the first sudden oak death science symposium held in Monterey in December 2002, it is amazing to see how far we...

Proceedings of the sudden oak death fifth science symposium

Treesearch

Susan J. Frankel; John T. Kliejunas; Katharine M. Palmieri; Janice M. Alexander

2013-01-01

The Proceedings of the Sudden Oak Death Fifth Science Symposium provides an update on research to address sudden oak death, caused by the exotic, quarantine pathogen, Phytophthora ramorum. Over 60 submissions present national and international investigations covering pathogen biology, biosecurity, genetics, monitoring, fire ecology, and diagnostics...

Phytophthora species from oak and tanoak forests in California and Oregon

Treesearch

Everett Hansen; David Rizzo; Matteo Garbelotto

2006-01-01

The current sudden oak death (SOD) epidemics in Europe and western North America triggered a search of North American oak forests for other Phytophthora species, and the results from the western United States have been surprising. Phytophthora ramorum has been the main quarry, and as an aerial pathogen, it is a surprise in itself....

Transduced human copper chaperone for Cu,Zn-SOD (PEP-1-CCS) protects against neuronal cell death.

PubMed

Choi, Soo Hyun; Kim, Dae Won; Kim, So Young; An, Jae Jin; Lee, Sun Hwa; Choi, Hee Soon; Sohn, Eun Jung; Hwang, Seok-Il; Won, Moo Ho; Kang, Tae-Cheon; Kwon, Hyung Joo; Kang, Jung Hoon; Cho, Sung-Woo; Park, Jinseu; Eum, Won Sik; Choi, Soo Young

2005-12-31

Reactive oxygen species (ROS) contribute to the development of various human diseases. Cu,Zn-superoxide dismutase (SOD) is one of the major means by which cells counteract the deleterious effects of ROS. SOD activity is dependent upon bound copper ions supplied by its partner metallochaperone protein, copper chaperone for SOD (CCS). In the present study, we investigated the protective effects of PEP-1-CCS against neuronal cell death and ischemic insults. When PEP-1-CCS was added to the culture medium of neuronal cells, it rapidly entered the cells and protected them against paraquat-induced cell death. Moreover, transduced PEP-1-CCS markedly increased endogenous SOD activity in the cells. Immunohistochemical analysis revealed that it prevented neuronal cell death in the hippocampus in response to transient forebrain ischemia. These results suggest that CCS is essential to activate SOD, and that transduction of PEP-1-CCS provides a potential strategy for therapeutic delivery in various human diseases including stroke related to SOD or ROS.

Effect of phosphate treatments on sudden oak death in tanoak and Shreve's oak

Treesearch

Doug Schmidt; Matteo Garbelotto; Dave Chambers; Steve Tjosvold

2006-01-01

Field experiments were conducted to evaluate the effectiveness of phosphonate chemical treatments for control of sudden oak death in tanoak (Lithocarpus densiflorus) and Shreve's oak (Quercus parvula var. Shrevei). Native stands of mature trees were preventatively treated with Agrifos® systemic fungicide and...

Sudden oak death in California: what is the potential?

Treesearch

Tara M. Barrett; Demetrios Gatziolis; Jeremy S. Fried; Karen L. Waddell

2006-01-01

Sudden oak death, a disease associated with the pathogen Phytophthora ramorum, has a large number of shrub and tree host species. Three of the tree species must susceptible to mortality from the disease, California black oak (Quercus kelloggii), coast live oak (Quercus agrifolia), and tanoak (...

A glimpse at future forests: predicting the effects of Phytophthora ramorum on oak forests of southern Appalachia

Treesearch

H.L. Spaulding; L.K. Rieske

2011-01-01

The highly pathogenic Phytophthora ramorum, causal organism of sudden oak death (SOD), is established in forests of the Pacific Northwest (USA) and is threatening invasion of other regions. Given the breadth of its host range, with dozens of asymptomatic ornamental hosts and with oaks, Quercus spp., in the red oak (Erythrobalanus) subgenus particularly susceptible, we...

Modeling risk for SOD nationwide: what are the effects of model choice on risk prediction?

Treesearch

M. Kelly; D. Shaari; Q. Guo; D. Liu

2006-01-01

Phytophthora ramorum has the potential to infect many forest types found throughout the United States. Efforts to model the potential habitat for P. ramorum and sudden oak death (SOD) are important for disease regulation and management. Yet, spatial models using identical data can have differing results. In this paper we examine...

Proceedings of the sudden oak death second science symposium: the state of our knowledge

Treesearch

Susan J. Frankel; Patrick J. Shea; Michael I. Haverty

2006-01-01

The Sudden Oak Death Second Science Symposium provided a forum for current research on sudden oak death, caused by the exotic, quarantine pathogen, Phytophthora ramorum. Ninety papers and forty-six posters on the following sudden oak death/P. ramorum topics are included: biology, genetics, nursery and wildland management,...

Sudden oak death and Phytophthora ramorum: a summary of the literature

Treesearch

John T. Kliejunas

2010-01-01

Sudden oak death and Phytophthora ramorum, both first recognized about a decade ago, have been the subject of hundreds of scientific and popular press articles. This document presents a comprehensive, concise summary of sudden oak death and P. ramorum research findings and management activities. Topics covered include...

Sudden oak death online symposium

Treesearch

S.D. Cohen; J., eds Juzwik

2003-01-01

This symposium is being made available to all who have an interest in the recent appearance of Sudden Oak Death, a plant disease with the potential to severely impact nursery growers, shippers, the lumber and wood products industry, landscapers, government programs and others. Scientific presentations dealing with the current status of the disease and ongoing research...

Phytophthora ramorum and sudden oak death in California: II. transmission and survival

Treesearch

Jennifer M. Davidson; David M. Rizzo; Matteo Garbelotto; Steven Tjosvold; Garey W. Slaughter

2002-01-01

The newly discovered Phytophthora ramorum canker disease of oak (Sudden Oak Death Syndrome) threatens millions of acres of California woodlands where coast live oak (Quercus agrifolia), tanoak (Lithocarpus densiflorus), or black oak (Quercus kelloggii) are dominant species. An important step in...

Relationships between Phytophthora ramorum canker (sudden oak death) and failure potential in coast live oak

Treesearch

Tedmund J. Swiecki; Elizabeth Bernhardt; Christiana Drake; Laurence R. Costello

2006-01-01

In autumn 2002, we conducted a retrospective study on coast live oak (Quercus agrifolia) failures in Marin County, California, woodlands affected by Phytophthora ramorum canker (sudden oak death). The objectives of this case-control study were to quantify levels of bole, large branch, and root failure in these woodlands and...

Mutant SOD1-expressing astrocytes release toxic factors that trigger motoneuron death by inducing hyperexcitability

PubMed Central

Fritz, Elsa; Izaurieta, Pamela; Weiss, Alexandra; Mir, Franco R.; Rojas, Patricio; Gonzalez, David; Rojas, Fabiola; Brown, Robert H.; Madrid, Rodolfo

2013-01-01

Amyotrophic lateral sclerosis (ALS) is a devastating paralytic disorder caused by dysfunction and degeneration of motoneurons starting in adulthood. Recent studies using cell or animal models document that astrocytes expressing disease-causing mutations of human superoxide dismutase 1 (hSOD1) contribute to the pathogenesis of ALS by releasing a neurotoxic factor(s). Neither the mechanism by which this neurotoxic factor induces motoneuron death nor its cellular site of action has been elucidated. Here we show that acute exposure of primary wild-type spinal cord cultures to conditioned medium derived from astrocytes expressing mutant SOD1 (ACM-hSOD1G93A) increases persistent sodium inward currents (PCNa), repetitive firing, and intracellular calcium transients, leading to specific motoneuron death days later. In contrast to TTX, which paradoxically increased twofold the amplitude of calcium transients and killed motoneurons, reduction of hyperexcitability by other specific (mexiletine) and nonspecific (spermidine and riluzole) blockers of voltage-sensitive sodium (Nav) channels restored basal calcium transients and prevented motoneuron death induced by ACM-hSOD1G93A. These findings suggest that riluzole, the only FDA-approved drug with known benefits for ALS patients, acts by inhibiting hyperexcitability. Together, our data document that a critical element mediating the non-cell-autonomous toxicity of ACM-hSOD1G93A on motoneurons is increased excitability, an observation with direct implications for therapy of ALS. PMID:23486205

A revised sudden oak death risk map to facilitate national surveys

Treesearch

Frank H. Koch; William D. Smith

2012-01-01

The impact of sudden oak death on Pacific Coast wildlands has received much attention from scientists, popular media, and the public. Disease symptoms were first observed in Marin County, in California, in 1994 on tanoak (Lithocarpus densiflorus) and, in 1995, on coast live oak (Quercus agrifolia) and California black oak (

Decay fungi of oaks and associated hardwoods for western arborists

Treesearch

Jessie A. Glaeser; Kevin T. Smith

2010-01-01

Examination of trees for the presence and extent of decay should be part of any hazard tree assessment. Identification of the fungi responsible for the decay improves prediction of tree performance and the quality of management decisions, including tree pruning or removal. Scouting for Sudden Oak Death (SOD) in the West has drawn attention to hardwood tree species,...

Phenotypic Diversification Is Associated with Host-Induced Transposon Derepression in the Sudden Oak Death Pathogen Phytophthora ramorum

PubMed Central

Kasuga, Takao; Kozanitas, Melina; Bui, Mai; Hüberli, Daniel; Rizzo, David M.; Garbelotto, Matteo

2012-01-01

The oomycete pathogen Phytophthora ramorum is responsible for sudden oak death (SOD) in California coastal forests. P. ramorum is a generalist pathogen with over 100 known host species. Three or four closely related genotypes of P. ramorum (from a single lineage) were originally introduced in California forests and the pathogen reproduces clonally. Because of this the genetic diversity of P. ramorum is extremely low in Californian forests. However, P. ramorum shows diverse phenotypic variation in colony morphology, colony senescence, and virulence. In this study, we show that phenotypic variation among isolates is associated with the host species from which the microbe was originally cultured. Microarray global mRNA profiling detected derepression of transposable elements (TEs) and down-regulation of crinkler effector homologs (CRNs) in the majority of isolates originating from coast live oak (Quercus agrifolia), but this expression pattern was not observed in isolates from California bay laurel (Umbellularia californica). In some instances, oak and bay laurel isolates originating from the same geographic location had identical genotypes based on multilocus simples sequence repeat (SSR) marker analysis but had different phenotypes. Expression levels of the two marker genes analyzed by quantitative reverse transcription PCR were correlated with originating host species, but not with multilocus genotypes. Because oak is a nontransmissive dead-end host for P. ramorum, our observations are congruent with an epi-transposon hypothesis; that is, physiological stress is triggered on P. ramorum while colonizing oak stems and disrupts epigenetic silencing of TEs. This then results in TE reactivation and possibly genome diversification without significant epidemiological consequences. We propose the P. ramorum-oak host system in California forests as an ad hoc model for epi-transposon mediated diversification. PMID:22529930

Sudden Oak Death, Phytophthora ramorum: A Persistent Threat to Oaks and Other Tree Species

Treesearch

S.J. Frankel; K.M. Palmieri

2014-01-01

This paper reviews the status and management of sudden oak death and “sudden larch death” in the urban and wildland forests of California, Oregon, and the UK. The causal pathogen, Phytophthora ramorum, was discovered in all three locations over a decade ago; however, efforts to contain and eliminate infestations have been unsuccessful. These less...

Sudden oak death: disease trends in Marin county plots after one year

Treesearch

Brice A. McPherson; David L. Wood; Andrew J. Storer; Nina Maggi Kelly; Richard B. Standiford

2002-01-01

Sudden oak death has emerged as a major threat to the oak forests of California. In oaks and tanoak, this disease complex consists of a previously unreported fungus-like pathogen, Phytophthora ramorum, insects (bark and ambrosia beetles), and a secondary fungus, Hypoxylon thouarsianum. Species monitored in this study were coast...

National Detection Surveys for Sudden Oak Death

Treesearch

B. M. Tkacz; S. W. Oak; W. D. Smith

2006-01-01

The Forest Health Monitoring program, a partnership of Federal and State forest management agencies, has developed and tested protocols for identifying and surveying forest ecosystems that may be vulnerable to invasion by Phytophthora ramorum, the cause of Sudden Oak Death in California and Oregon. This detection survey is targeting areas outside the currently known...

Astrocytes expressing mutant SOD1 and TDP43 trigger motoneuron death that is mediated via sodium channels and nitroxidative stress

PubMed Central

Rojas, Fabiola; Cortes, Nicole; Abarzua, Sebastian; Dyrda, Agnieszka; van Zundert, Brigitte

2013-01-01

Amyotrophic lateral sclerosis (ALS) is a fatal paralytic disorder caused by dysfunction and degeneration of motor neurons. Multiple disease-causing mutations, including in the genes for SOD1 and TDP-43, have been identified in ALS. Astrocytes expressing mutant SOD1 are strongly implicated in the pathogenesis of ALS: we have shown that media conditioned by astrocytes carrying mutant SOD1G93A contains toxic factor(s) that kill motoneurons by activating voltage-sensitive sodium (Nav) channels. In contrast, a recent study suggests that astrocytes expressing mutated TDP43 contribute to ALS pathology, but do so via cell-autonomous processes and lack non-cell-autonomous toxicity. Here we investigate whether astrocytes that express diverse ALS-causing mutations release toxic factor(s) that induce motoneuron death, and if so, whether they do so via a common pathogenic pathway. We exposed primary cultures of wild-type spinal cord cells to conditioned medium derived from astrocytes (ACM) that express SOD1 (ACM-SOD1G93A and ACM-SOD1G86R) or TDP43 (ACM-TDP43A315T) mutants; we show that such exposure rapidly (within 30–60 min) increases dichlorofluorescein (DCF) fluorescence (indicative of nitroxidative stress) and leads to extensive motoneuron-specific death within a few days. Co-application of the diverse ACMs with anti-oxidants Trolox or esculetin (but not with resveratrol) strongly improves motoneuron survival. We also find that co-incubation of the cultures in the ACMs with Nav channel blockers (including mexiletine, spermidine, or riluzole) prevents both intracellular nitroxidative stress and motoneuron death. Together, our data document that two completely unrelated ALS models lead to the death of motoneuron via non-cell-autonomous processes, and show that astrocytes expressing mutations in SOD1 and TDP43 trigger such cell death through a common pathogenic pathway that involves nitroxidative stress, induced at least in part by Nav channel activity. PMID:24570655

Responses of oaks and tanoaks to the sudden oak death pathogen after 8 y of monitoring in two coastal California forests

Treesearch

Brice A. McPherson; Sylvia R. Mori; David L. Wood; Maggi Kelly; Andrew J. Storer; Pavel Svihra; Richard B. Standiford

2010-01-01

Sudden oak death, caused by Phytophthora ramorum, is widely established in mesic forests of coastal central and northern California. In 2000, we placed 18 plots in two Marin County sites to monitor disease progression in coast live oaks (Quercus agrifolia), California black oaks (Q. kelloggii), and tanoaks (Lithocarpus densiflorus), the species that are most...

Decay fungi associated with oaks and other hardwoods in the western United States

Treesearch

Jessie A. Glaeser; Kevin T. Smith

2010-01-01

An assessment of the presence and extent of the wood decay process should be part of any hazard tree analysis. Identification of the fungi responsible for decay improves both the prediction of the consequences of wood decay and the prescription of management options including tree pruning or removal. Until the outbreak of Sudden Oak Death (SOD), foresters in the...

Temporal epidemiology of sudden oak death in Oregon

Treesearch

Ebba K. Peterson; Everett M. Hansen; Alan Kanaskie

2015-01-01

An effort to eradicate Phytophthora ramorum, causal agent of sudden oak death, has been underway since its discovery in Oregon forests. Using an information-theoretical approach, we sought to model yearly variation in the size of newly infested areas and dispersal distance. Maximum dispersal distances were best modeled by spring and winter...

Disease risk factors and disease progress in coast live oak and tanoak affected by Phytophthora ramorum canker (sudden oak death)

Treesearch

Tedmund J. Swiecki; Elizabeth Bernhardt

2006-01-01

This paper reports on five years of observations in a case-control study examining the role of tree and site factors on the development of Phytophthora ramorum stem canker (sudden oak death) in coast live oak (Quercus agrifolia) and tanoak (Lithocarpus densiflorus). In September of each year from 2000 through...

Emergence of the sudden oak death pathogen Phytophthora ramorum

Treesearch

Niklaus J. Grunwald; Matteo Garbelotto; Erica M. Goss; Kurt Huengens; Simone Prospero

2012-01-01

The recently emerged plant pathogen Phytophthora ramorum is responsible for causing the sudden oak death epidemic. This review documents the emergence of P. ramorum based on evolutionary and population genetic analyses. Currently infection by P. ramorum occurs only in Europe and North America and three...

GSOB ≠ SOD. Tree mortality from the goldspotted oak borer in oak woodlands of southern California.

Treesearch

Tom W. Coleman; Steven J. Seybold

2010-01-01

A new threat to oaks (Quercus spp.) in California was identified in June 2008 following years of misdiagnosis. The goldspotted oak borer (GSOB), Agrilus coxalis auroguttatus Schaeffer (Coleoptera: Buprestidae), is aggressively attacking and killing three species of oaks in oak woodlands in San Diego County. About 20,000...

Searching for early-warning signals of impending dieback and death in Mediterranean oaks

NASA Astrophysics Data System (ADS)

Colangelo, Michele; Ripullone, Francesco; Julio Camarero, Jesus; De Micco, Veronica; Gazol, Antonio; Gentilesca, Tiziana; Borghetti, Marco

2017-04-01

In recent decades, forest dieback episodes have been recorded worldwide affecting different tree species. In particular, several cases of widespread dieback and increased mortality rates have been described for Mediterranean oak (Quercus spp.) species. These dieback cases are revealing the high vulnerability of Mediterranean oaks, manifested as a loss in tree vigour (leaf shedding, canopy and shoot dieback), growth decline and sometimes tree death, as a consequence of temperatures rising at unprecedented rates and drying trends. However, in the wake of the so-called 'oak decline phenomenon', the attention on these species has generally been limited, perhaps because they are often regarded as well-adapted to the dry conditions typical of Mediterranean areas. Indeed, according to recent studies, the reduced size, the ability to sprout and the anisohydric behavior of Mediterranean oak species (reduced control of water loss and high stomatal conductance rates) would make them better adapted to withstand heat and drought stress then taller and non-sprouting isohydric species (e.g. conifer, with strict control of water loss by closing stomata). Here, we investigated the vulnerability of Mediterranean oaks by comparing neighboring living and recently dead trees in species with low (Q. pubescens), intermediate (Q. cerris, Q. frainetto) and high (Q. robur) sensitivity to water shortage. We analysed changes in tree vigour using tree-ring width and functional wood anatomical traits as proxies to search for early-warning signals of dieback, in connection with the main proposed dieback mechanisms (hydraulic failure and/or carbon starvation). We also modeled the probability of tree death as a function of tree size (diameter, height) by quantifying recent changes in growth and wood anatomy along tree-ring series. Contrary to the general concept that trees tend to experience increasing cavitation risk with increasing height, our studies show that smaller oaks are more prone to die

Susceptibility to Phytophthora ramorum in California bay laurel, a key foliar host of sudden oak death

Treesearch

Brian L. Anacker; Nathan E. Rank; Daniel Hüberli; Matteo Garbelotto; Sarah Gordon; Rich Whitkus; Tami Harnik; Matthew Meshriy; Lori Miles; Ross K. Meentemeyer

2008-01-01

Sudden oak death, caused by the water mold Phytophthora ramorum, is a plant disease responsible for the death of hundreds of thousands of oak and tanoak trees. Some foliar hosts play a major role in the epidemiology of this disease. Upon infection by P. ramorum, these foliar hosts express non-fatal leaf lesions from which large...

Linking sudden oak death with spatial economic value transfer

Treesearch

Tom Holmes; Bill Smith

2008-01-01

Sudden oak death (caused by Phytophthora ramorum) is currently having a dramatic impact on the flow of ecosystem services provided by trees and forests in California. Timber species in California are not thought to be at risk of mortality from this pathogen and, consequently, economic impacts accrue to non-market values of trees such as aesthetics,...

Sudden oak death: recent developments on trees in Europe

Treesearch

Clive Brasier; Sandra Denman; Joan Webber; Anna Brown

2006-01-01

In November 2000 a new Phytophthora originally found on rhododendron stock in Germany and the Netherlands in 1993 and the new Phytophthora believed to be the cause of sudden oak death in California were shown to be the same organism. This development led to a summary Pest Risk Analysis (PRA) for Europe being prepared by Forest...

Innovation and dedication underpin management of sudden oak death (Phytophthora ramorum) in California and Oregon forests

Treesearch

Susan J. Frankel

2017-01-01

This special issue of Forest Phytophthoras serves as part of the proceedings from the Sixth Sudden Oak Death Science Symposium held June 21 -23, 2016 at Fort Mason Center in San Francisco, CA, USA. The symposium marked almost 16 years to the day that David Rizzo (UC Davis) and Matteo Garbelotto (UC Berkeley) identified the cause of sudden oak death to be a previously...

The dynamic response of housing values to a forst invasive disease: evidence from a sudden oak death infestation

Treesearch

Kent Kovacs; Thomas P. Holmes; Jeffrey E. Englin; Janice Alexander

2011-01-01

"Sudden Oak Death" (Phytophthora ramorum) is a non-indigenous forest pathogen which causes substantialmortality of coast live oak (Quercus agrifolia) and several other oak tree species on the Pacific Coast of the United States. We estimated the time path of residential property values subject to oak mortality using a...

Sudden oak death effects on the dynamics of dead wood

Treesearch

Richard C. Cobb; Jo& atilde; o Filipe A.N.; Margaret R. Metz; Ross K. Meentemeyer; David M. Rizzo

2013-01-01

Sudden oak death has impacted forests notable for high-fire risk and contiguous host communities in California and Oregon coastal forest ecosystems. The disease continues to emerge in stands and landscapes with a large biomass of tanoak (Notholithocarpus densiflorus (Hook.&Arn.) Manos, Cannon & S.H.Oh), and we show that woody debris also...

Surveying and monitoring sudden oak death in southwest Oregon forests

Treesearch

Ellen Michaels Goheen; Alan Kanaskie; Mike McWilliams; Everett Hansen; Wendy Sutton; Nancy Osterbauer

2006-01-01

Phytophthora ramorum, the causal agent of sudden oak death, was first discovered in Oregon in July 2001 by aerial survey (Goheen and others 2002). Alerted to the situation in California and experienced in aerial tree mortality surveys, cooperators from the USDA Forest Service and the Oregon Department of Forestry planned a pilot survey for P...

PGC-1α/ERRα-Sirt3 Pathway Regulates DAergic Neuronal Death by Directly Deacetylating SOD2 and ATP Synthase β

PubMed Central

Zhang, Xuefei; Ren, Xiaoqing; Zhang, Qi; Li, Zheyi; Ma, Shuaipeng; Bao, Jintao; Li, Zeyang; Bai, Xue; Zheng, Liangjun; Zhang, Zhong; Shang, Shujiang; Zhang, Chen; Wang, Chuangui; Cao, Liu

2016-01-01

Abstract Aims: Parkinson's disease (PD) heavily affects humans and little is known about its cause and pathogenesis. Sirtuin 3 (Sirt3) plays a key role in regulating mitochondrial dysfunction, which is the main cause of DAergic neuronal loss in PD. We investigated the mechanisms of neuroprotective role of Sirt3 in DAergic neuronal survival. Results: Sirt3 was reduced in 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP)-treated neurons with its overexpression being neuroprotective. We identified that Sirt3 interacted with manganese superoxide dismutase (SOD2) and adenosine triphosphate (ATP) synthase β and modulated their activities by deacetylating SOD2 (K130) and ATP synthase β (K485) to prevent reactive oxygen species accumulation and ATP depletion, and to alleviate DAergic neuronal death upon MPTP treatment. Peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) interacted with estrogen-related receptor alpha (ERRα) that bound to the Sirt3 promoter as its transcription factor to regulate Sirt3 expression and DAergic neuronal death. In the mouse midbrain, MPTP administration led to the loss of PGC-1α and Sirt3, high acetylation level of SOD2 and ATP synthase β, and the specific loss of DAergic neurons, while Sirt3 overexpression could protect against DAergic neuronal loss. Sirt3 knockout mice exhibited more sensitive and more DAergic neuronal loss to MPTP treatment. Innovation: The study provides new insights into a critical PGC-1α/ERRα-Sirt3 pathway, linking regulation of mitochondrial protein acetylation and DAergic neuronal death in PD pathogenesis, which provide a potential therapeutic strategy and target in PD treatment. Conclusion: These results provide a vital PGC-1α/ERRα-Sirt3 pathway that protects against DAergic neuronal death by directly deacetylating SOD2 (K130) and ATP synthase β (K485) in PD. Antioxid. Redox Signal. 24, 312–328. PMID:26421366

Oak Decline

Treesearch

Philip M. Wargo; David R. Houston; Leon A. LaMadeleine

1983-01-01

Periodic occurrences of decline and death of oaks over widespread areas have been recorded since 1900. These outbreaks, variously named oak decline, oak dieback, or oak mortality, are caused by a complex interaction of environmental stresses and pests and given the name oak decline.

Predicting the economic costs and property value losses attributed to sudden oak death damage in California (2010-2020)

Treesearch

Kent Kovacs; Tomas Václavík; Robert G. Haight; Arwin Pang; Nik J. Cunniffe; Christopher A. Gilligan; Ross K. Meentemeyer

2011-01-01

Phytophthora ramorum, cause of sudden oak death, is a quarantined, non-native, invasive forest pathogen resulting in substantial mortality in coastal live oak (Quercus agrifolia) and several other related tree species on the Pacific Coast of the United States. We estimate the discounted cost of oak treatment, removal, and...

The dynamic response of housing values to a forest invasive disease: evidence from a sudden oak death infestation

Treesearch

Kent Kovacs; Thomas P Holmes; Jeffrey E Englin; Janice Alexander

2011-01-01

“Sudden Oak Death” (Phytophthora ramorum) is a non-indigenous forest pathogen which causes substantial mortality of coast live oak (Quercus agrifolia) and several other oak tree species on the Pacific Coast of the United States. We estimated the time path of residential property values subject to oak mortality using a dataset that spans more than two decades—including...

Decomposition and N cycling changes in redwood forests caused by sudden oak death

Treesearch

Richard C. Cobb; David M. Rizzo

2012-01-01

Phytophthora ramorum is an emergent pathogen in redwood forests which causes the disease sudden oak death. Although the disease does not kill coast redwood (Sequoia sempervirens), extensive and rapid mortality of tanoak (Notholithocarpus densiflorus) has removed this...

Slowing spread of sudden oak death in Oregon forests, 2001–2015

Treesearch

Alan Kanaskie; Randy Wiese; Danny Norlander; Jon Laine; Sarah Navarro; Ellen Michaels Goheen; Ron Rhatigan; Everett Hansen; Wendy Sutton; Paul Reeser; Nik Grunwald; Zhian Kamvar; Nancy Osterbauer

2017-01-01

Sudden oak death, caused by Phytophthora ramorum, is lethal to tanoak (Notholithocarpus densiflorus) and threatens this species throughout its range in Oregon. The disease was first discovered in coastal southwest Oregon forests in July 2001. An interagency team attempted to eradicate the pathogen through a program of...

Regeneration and tanoak mortality in coast redwood stands affected by sudden oak death

Treesearch

Benjamin S. Ramage; Kevin L. OHara; Alison B. Forreste

2012-01-01

Sudden oak death, an emerging disease caused by the exotic pathogen Phytophthora ramorum, is impacting coast redwood (Sequoia sempervirens) forests throughout coastal California. The most severely affected species, tanoak (Notholithocarpus densiflorus), is currently widespread and abundant in the redwood...

Calpastatin inhibits motor neuron death and increases survival of hSOD1(G93A) mice.

PubMed

Rao, Mala V; Campbell, Jabbar; Palaniappan, Arti; Kumar, Asok; Nixon, Ralph A

2016-04-01

Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron disease with a poorly understood cause and no effective treatment. Given that calpains mediate neurodegeneration in other pathological states and are abnormally activated in ALS, we investigated the possible ameliorative effects of inhibiting calpain over-activation in hSOD1(G93A) transgenic (Tg) mice in vivo by neuron-specific over-expression of calpastatin (CAST), the highly selective endogenous inhibitor of calpains. Our data indicate that over-expression of CAST in hSOD1(G93A) mice, which lowered calpain activation to levels comparable to wild-type mice, inhibited the abnormal breakdown of cytoskeletal proteins (spectrin, MAP2 and neurofilaments), and ameliorated motor axon loss. Disease onset in hSOD1(G93A) /CAST mice compared to littermate hSOD1(G93A) mice is delayed, which accounts for their longer time of survival. We also find that neuronal over-expression of CAST in hSOD1(G93A) transgenic mice inhibited production of putative neurotoxic caspase-cleaved tau and activation of Cdk5, which have been implicated in neurodegeneration in ALS models, and also reduced the formation of SOD1 oligomers. Our data indicate that inhibition of calpain with CAST is neuroprotective in an ALS mouse model. CAST (encoding calpastatin) inhibits hyperactivated calpain to prevent motor neuron disease operating through a cascade of events as indicated in the schematic, with relevance to amyotrophic lateral sclerosis (ALS). We propose that over-expression of CAST in motor neurons of hSOD1(G93A) mice inhibits activation of CDK5, breakdown of cytoskeletal proteins (NFs, MAP2 and Tau) and regulatory molecules (Cam Kinase IV, Calcineurin A), and disease-causing proteins (TDP-43, α-Synuclein and Huntingtin) to prevent neuronal loss and delay neurological deficits. In our experiments, CAST could also inhibit cleavage of Bid, Bax, AIF to prevent mitochondrial, ER and lysosome-mediated cell death mechanisms. Similarly, CAST

Analysis of populations of the sudden oak death pathogen in Oregon forests

Treesearch

Zhian N. Kamvar; Everett M. Hansen; Alan M. Kanaskie; Meredith M. Larsen; Niklaus J. Grünwald

2017-01-01

Sudden oak death, caused by the oomycete Phytophthora ramorum, was first discovered in California toward the end of the 20th century and subsequently emerged on tanoak forests in Oregon before its first detection in 2001 by aerial surveys. The Oregon Department of Forestry has since monitored the epidemic and sampled symptomatic tanoak trees from...

Modeling when, where, and how to manage a forest epidemic, motivated by sudden oak death in California

Treesearch

Nik J. Cunniffe; Richard C. Cobb; Ross K. Meentemeyer; David M. Rizzo; Christopher A. Gilligan

2016-01-01

Sudden oak death, caused by Phytophthora ramorum, has killed millions of oak and tanoak in California since its first detection in 1995. Despite some localized small-scale management, there has been no large-scale attempt to slow the spread of the pathogen in California. Here we use a stochastic spatially-explicit model parameterized using data on...

Examining the relationship between fire history and sudden oak death patterns: a case study in Sonoma County

Treesearch

Max A. Moritz; Dennis C. Odion

2006-01-01

Fire is often integral to forest ecology and can affect forest disease dynamics. Sudden oak death has spread across a large, fire-prone portion of California, killing large numbers of oaks and tanoaks and infecting most associated woody plants. Building on our earlier study of fire-disease dynamics, we examined spatial patterns of confirmed infections in relation to...

Mapping sudden oak death risk nationally using host, climate, and pathways data

Treesearch

Frank H. Koch; William D. Smith

2008-01-01

In 2002, a team of United States Department of Agriculture-Forest Service (USDA-FS) scientists developed a preliminary risk map to serve as the foundation for an efficient, cost effective sample design for the national sudden oak death detection survey. At the time, a need to initiate rapid detection in the face of limited information on Phytophthora ramorum...

Genetic epidemiology of the Sudden Oak Death pathogen Phytophthora ramorum in California

Treesearch

S. Mascheretti; P.J.P. Croucher; M. Kozanitas; L. Baker; M. Garbelotto

2009-01-01

A total of 669 isolates of Phytophthora ramorum, the pathogen responsible for Sudden Oak Death, were collected from 34 Californian forests and from the ornamental plant-trade. Seven microsatellite markers revealed 82 multilocus genotypes (MGs) of which only three were abundant (>10%). Iteratively collapsing based upon minimum ΦST, yielded five meta-samples and five...

Ancient isolation and independent evolution of the three clonal lineages of the exotic sudden oak death pathogen Phytophthora ramorum

Treesearch

E.M. Goss; I. Carbone; N.J. Grünwald

2009-01-01

The genus Phytophthora includes some of the most destructive plant pathogens affecting agricultural and native ecosystems and is responsible for a number of recent emerging and re-emerging infectious diseases of plants. Sudden oak death, caused by the exotic pathogen P. ramorum, has caused extensive mortality of oaks...

Managing sudden oak death on federal lands in southwest Oregon: triumphs and challenges

Treesearch

Ellen Michaels Goheen

2017-01-01

Since 2001, approximately 5,350 acres of tanoak forests in Curry County, Oregon have been treated to eradicate Phytophthora ramorum and slow the spread of sudden oak death. Over 1,300 of these acres are on lands administered by the USDI Bureau of Land Management (BLM CB), Coos Bay District and the USDA Forest Service, Rogue River-Siskiyou...

Standardizing the Nomenclature for Clonal Lineages of the Sudden Oak Death Pathogen, Phytophthora ramorum

USDA-ARS?s Scientific Manuscript database

Phytophthora ramorum, the causal agent of sudden oak death and ramorum blight, is known to exist as three distinct clonal lineages based on a range of molecular marker systems. However, in the recent literature there exists no consensus on naming of lineages. Here we name clonal lineages of P. ramor...

Quantification of sudden oak death tree mortality in the Big Sur ecoregion of California

Treesearch

Douglas A. Shoemaker; Christopher B. Oneal; David M. Rizzo; Ross K. Meentemeyer

2008-01-01

Big Sur is one of the most ecologically diverse regions in California and well recognized as a biodiversity hotspot for global conservation priority. Currently the region is experiencing substantial environmental change due to the invasion of Phytophthora ramorum, the plant pathogen causing the forest disease known as sudden oak death. First...

Oak wilt and oak decline in the upper midwest USA

Treesearch

Jennifer Juzwik; Thomas L. Schmidt

2000-01-01

Oaks are a significant component of the hardwood forests of the Upper Midwest USA. Numerous species occur over vast areas in the region and are highly valued for a variety of reasons. Oak wilt caused by C. fagacearum, and oak decline associated with several factors are the major causes of the species, deterioration and death in the region....

The social impacts of sudden oak death and other forest diseases: a panel discussion

Treesearch

Janice Alexander; Chris Lee

2010-01-01

This panel aimed to discuss the intersection of biology and society; specifically, how we balance competing social and biological concerns in regards to forest pests and land management in general. Four panelists began the discussion: Janice Alexander, Sudden Oak Death Outreach Coordinator for the University of California (U.C.) Cooperative Extension, Marin County and...

Standardizing the nomenclature for clonal lineages of the sudden oak death pathogen, Phytophthora ramorum

Treesearch

N.J. Grünwald; E.M. Goss; K. Ivors; M. Garbelotto; F.N. Martin; S. Prospero; E. Hansen; P.J.M. Bonants; R.C. Hamelin; G. Chastagner; S. Werres; D.M. Rizzo; G. Abad; P. Beales; G.J. Bilodeau; C.L. Blomquist; C. Brasier; S.C. Brière; A. Chandelier; J.M. Davidson; S. Denman; M. Elliott; S.J. Frankel; E.M. Goheen; H. de Gruyter; K. Heungens; D. James; A. Kanaskie; M.G. McWilliams; W. Man in ' t Veld; E. Moralejo; N.K. Osterbauer; M.E. Palm; J.L. Parke; A.M. Perez Sierra; S.F. Shamoun; N. Shishkoff; P.W. Tooley; A.M. Vettraino; J. Webber; T.L. Widmer

2009-01-01

Phytophthora ramorum, the causal agent of sudden oak death and ramorum blight, is known to exist as three distinct clonal lineages which can only be distinguished by performing molecular marker-based analyses. However, in the recent literature there exists no consensus on naming of these lineages. Here we propose a system for naming clonal lineages of P. ramorum based...

Spatial relationship between Phytophthora ramorum and roads or streams in Oregon tanoak forests

Treesearch

Ebba Peterson; Everett Hansen; Alan Kanaskie

2014-01-01

The pathogen, Phytophthora ramorum, causal agent of sudden oak death (SOD) of oaks and tanoaks, continues to expand its range within Oregon despite an effort to eradicate it from native forests. With its early detection and prompt removal of infected hosts, the Oregon SOD eradication program has produced a landscape distribution of disease...

Large SOD1 aggregates, unlike trimeric SOD1, do not impact cell viability in a model of amyotrophic lateral sclerosis.

PubMed

Zhu, Cheng; Beck, Matthew V; Griffith, Jack D; Deshmukh, Mohanish; Dokholyan, Nikolay V

2018-05-01

Aberrant accumulation of misfolded Cu, Zn superoxide dismutase (SOD1) is a hallmark of SOD1-associated amyotrophic lateral sclerosis (ALS), an invariably fatal neurodegenerative disease. While recent discovery of nonnative trimeric SOD1-associated neurotoxicity has suggested a potential pathway for motor neuron impairment, it is yet unknown whether large, insoluble aggregates are cytotoxic. Here we designed SOD1 mutations that specifically stabilize either the fibrillar form or the trimeric state of SOD1. The designed mutants display elevated populations of fibrils or trimers correspondingly, as demonstrated by gel filtration chromatography and electron microscopy. The trimer-stabilizing mutant, G147P, promoted cell death, even more potently in comparison with the aggressive ALS-associated mutants A4V and G93A. In contrast, the fibril-stabilizing mutants, N53I and D101I, positively impacted the survival of motor neuron-like cells. Hence, we conclude the SOD1 oligomer and not the mature form of aggregated fibril is critical for the neurotoxic effects in the model of ALS. The formation of large aggregates is in competition with trimer formation, suggesting that aggregation may be a protective mechanism against formation of toxic oligomeric intermediates.

Evidence for the role of synchronicity between host phenology and pathogen activity in the distribution of sudden oak death canker disease.

PubMed

Dodd, Richard S; Hüberli, Daniel; Mayer, Wasima; Harnik, Tamar Y; Afzal-Rafli, Zara; Garbelotto, Matteo

2008-07-01

Variations in synchronicity between colonization rate by the pathogen and host phenology may account for unexplained spatial distribution of canker disease. The hypothesis that synchronous pathogenicity and host development are necessary for incidence of sudden oak death disease was tested by correlating seasonal variations in host cambial phenology and response to inoculation with Phytophthora ramorum. Response to infection was estimated by inoculating branch cuttings from coast live oak (Quercus agrifolia) trees at nine dates through a full annual cycle in 2003-2004. Host phenology was estimated from measurements of bud burst and cambial activity in spring 2006. Lesions were largest in the spring soon after the cambium resumed activity. A moderate genetic component to lesion size was detected. Variation among trees in date of largest lesions correlated with variation in timing of bud burst and cambial phenology. The data support the hypothesis that active host cambial tissue is a necessary requisite for successful infection with the pathogen that causes sudden oak death canker disease. Genetic variation in host phenology will buffer coast live oak against epidemics of this disease.

Expression and Distribution of Arylsulfatase B are Closely Associated with Neuron Death in SOD1 G93A Transgenic Mice.

PubMed

Zhang, Jie; Liang, Huiting; Zhu, Lei; Gan, Weiming; Tang, Chunyan; Li, Jiao; Xu, Renshi

2018-02-01

The known proteins only explained the partial pathogenesis of amyotrophic lateral sclerosis (ALS). Therefore, this study aimed to search the novel proteins possibly involved in ALS. In this study, we analyzed the expression and distribution of the candidate protein arylsulfatase B (ARSB) in the different segments, anatomic regions, and neural cells of spinal cord at the different stages of the wild-type and [Cu/Zn] superoxide dismutase 1 (SOD1) G93A transgenic mice using the fluorescent immunohistochemistry and the western blot. The results revealed that the ARSB was extensively expressed and distributed in the entire spinal cord; the expression and distribution of ARSB was significantly different in the different regions of spinal cord, the anterior horn of gray matter (AHGM) was significantly more than that in the posterior horn of gray matter (PHGM) and significantly more than that in the central canal, and ARSB was mainly distributed in the microglia and neuron cells in the wild-type mice. The expression of ARSB significantly increased in other anatomic regions besides the thoracic PHGM, significantly decreased at the progression stage, occurred in the redistribution from the AHGM and the PHGM to the central canal at the onset and progression stages, and no any alteration of ARSB expression and distribution occurred between the different neural cells in the SOD1 G93A mice compared with the wild-type mice. The increase of ARSB expression and distribution followed with the increased of neuron death. Our data suggested that the abnormal expression and distribution of ARSB were closely associated with the neuron death in the SOD1 G93A transgenic mice.

Host-induced aneuploidy and phenotypic diversification in the Sudden Oak Death pathogen Phytophthora ramorum.

PubMed

Kasuga, Takao; Bui, Mai; Bernhardt, Elizabeth; Swiecki, Tedmund; Aram, Kamyar; Cano, Liliana M; Webber, Joan; Brasier, Clive; Press, Caroline; Grünwald, Niklaus J; Rizzo, David M; Garbelotto, Matteo

2016-05-20

Aneuploidy can result in significant phenotypic changes, which can sometimes be selectively advantageous. For example, aneuploidy confers resistance to antifungal drugs in human pathogenic fungi. Aneuploidy has also been observed in invasive fungal and oomycete plant pathogens in the field. Environments conducive to the generation of aneuploids, the underlying genetic mechanisms, and the contribution of aneuploidy to invasiveness are underexplored. We studied phenotypic diversification and associated genome changes in Phytophthora ramorum, a highly destructive oomycete pathogen with a wide host-range that causes Sudden Oak Death in western North America and Sudden Larch Death in the UK. Introduced populations of the pathogen are exclusively clonal. In California, oak (Quercus spp.) isolates obtained from trunk cankers frequently exhibit host-dependent, atypical phenotypes called non-wild type (nwt), apparently without any host-associated population differentiation. Based on a large survey of genotypes from different hosts, we previously hypothesized that the environment in oak cankers may be responsible for the observed phenotypic diversification in P. ramorum. We show that both normal wild type (wt) and nwt phenotypes were obtained when wt P. ramorum isolates from the foliar host California bay (Umbellularia californica) were re-isolated from cankers of artificially-inoculated canyon live oak (Q. chrysolepis). We also found comparable nwt phenotypes in P. ramorum isolates from a bark canker of Lawson cypress (Chamaecyparis lawsoniana) in the UK; previously nwt was not known to occur in this pathogen population. High-throughput sequencing-based analyses identified major genomic alterations including partial aneuploidy and copy-neutral loss of heterozygosity predominantly in nwt isolates. Chromosomal breakpoints were located at or near transposons. This work demonstrates that major genome alterations of a pathogen can be induced by its host species. This is an

Reduced mitochondrial SOD displays mortality characteristics reminiscent of natural aging

PubMed Central

Paul, Anirban; Belton, Amy; Nag, Sanjay; Martin, Ian; Grotewiel, Michael S.; Duttaroy, Atanu

2009-01-01

Manganese superoxide dismutase (MnSOD or SOD2) is a key mitochondrial enzymatic antioxidant. Arguably the most striking phenotype associated with complete loss of SOD2 in flies and mice is shortened life span. To further explore the role of SOD2 in protecting animals from aging and age-associated pathology, we generated a unique collection of Drosophila mutants that progressively reduce SOD2 expression and function. Mitochondrial aconitase activity was substantially reduced in the Sod2 mutants, suggesting that SOD2 normally ensures the functional capacity of mitochondria. Flies with severe reductions in SOD2 expression exhibited accelerated senescence of olfactory behavior as well as precocious neurodegeneration and DNA strand breakage in neurons. Furthermore, life span was progressively shortened and age-dependent mortality was increased in conjunction with reduced SOD2 expression, while initial mortality and developmental viability were unaffected. Interestingly, life span and age-dependent mortality varied exponentially with SOD2 activity, indicating that there might normally be a surplus of this enzyme for protecting animals from premature death. Our data support a model in which disruption of the protective effects of SOD2 on mitochondria manifests as profound changes in behavioral and demographic aging as well as exacerbated age-related pathology in the nervous system. PMID:18078670

Phytophthora ramorum infection in coast live oaks and Shreve's oaks treated with insecticide to prevent beetle colonization

Treesearch

Brice A. McPherson; David L. Wood; David M. Rizzo; Pavel Svihra; Steve Tjosvold; Andrew J. Storer; Richard B. Standiford

2006-01-01

As the name implies, sudden oak death, caused by Phytophthora ramorum, kills many, if not most of the coast live oaks, Quercus agrifolia, that become infected (McPherson and others, 2005). Several genera of ambrosia and bark beetles (Coleoptera: Scolytidae) colonize bleeding (infected) trees and are suspected to hasten tree death....

Long-term monitoring of sudden oak death in Marin County and the East Bay Hills

Treesearch

Brice A. McPherson; Greg Biging; Maggi Kelly; David L. Wood

2017-01-01

Prior to 2000 the etiology, effects on host trees, and possible consequences for northern California’s forests of the syndrome known as sudden oak death were unknown. We designed a plot-based study to address these issues and to set a baseline for future evaluations.In March-April 2000 we established a total of 20 plots in two forested...

The TrkAIII oncoprotein inhibits mitochondrial free radical ROS-induced death of SH-SY5Y neuroblastoma cells by augmenting SOD2 expression and activity at the mitochondria, within the context of a tumour stem cell-like phenotype.

PubMed

Ruggeri, Pierdomenico; Farina, Antonietta R; Di Ianni, Natalia; Cappabianca, Lucia; Ragone, Marzia; Ianni, Giulia; Gulino, Alberto; Mackay, Andrew R

2014-01-01

The developmental and stress-regulated alternative TrkAIII splice variant of the NGF receptor TrkA is expressed by advanced stage human neuroblastomas (NBs), correlates with worse outcome in high TrkA expressing unfavourable tumours and exhibits oncogenic activity in NB models. In the present study, we report that constitutive TrkAIII expression in human SH-SY5Y NB cells inhibits Rotenone, Paraquat and LY83583-induced mitochondrial free radical reactive oxygen species (ROS)-mediated death by stimulating SOD2 expression, increasing mitochondrial SOD2 activity and attenuating mitochondrial free radical ROS production, in association with increased mitochondrial capacity to produce H2O2, within the context of a more tumour stem cell-like phenotype. This effect can be reversed by the specific TrkA tyrosine kinase inhibitor GW441756, by the multi-kinase TrkA inhibitors K252a, CEP-701 and Gö6976, which inhibit SOD2 expression, and by siRNA knockdown of SOD2 expression, which restores the sensitivity of TrkAIII expressing SH-SY5Y cells to Rotenone, Paraquat and LY83583-induced mitochondrial free radical ROS production and ROS-mediated death. The data implicate the novel TrkAIII/SOD2 axis in promoting NB resistance to mitochondrial free radical-mediated death and staminality, and suggest that the combined use of TrkAIII and/or SOD2 inhibitors together with agents that induce mitochondrial free radical ROS-mediated death could provide a therapeutic advantage that may also target the stem cell niche in high TrkA expressing unfavourable NB.

The TrkAIII Oncoprotein Inhibits Mitochondrial Free Radical ROS-Induced Death of SH-SY5Y Neuroblastoma Cells by Augmenting SOD2 Expression and Activity at the Mitochondria, within the Context of a Tumour Stem Cell-like Phenotype

PubMed Central

Di Ianni, Natalia; Cappabianca, Lucia; Ragone, Marzia; Ianni, Giulia; Gulino, Alberto; Mackay, Andrew R.

2014-01-01

The developmental and stress-regulated alternative TrkAIII splice variant of the NGF receptor TrkA is expressed by advanced stage human neuroblastomas (NBs), correlates with worse outcome in high TrkA expressing unfavourable tumours and exhibits oncogenic activity in NB models. In the present study, we report that constitutive TrkAIII expression in human SH-SY5Y NB cells inhibits Rotenone, Paraquat and LY83583-induced mitochondrial free radical reactive oxygen species (ROS)-mediated death by stimulating SOD2 expression, increasing mitochondrial SOD2 activity and attenuating mitochondrial free radical ROS production, in association with increased mitochondrial capacity to produce H2O2, within the context of a more tumour stem cell-like phenotype. This effect can be reversed by the specific TrkA tyrosine kinase inhibitor GW441756, by the multi-kinase TrkA inhibitors K252a, CEP-701 and Gö6976, which inhibit SOD2 expression, and by siRNA knockdown of SOD2 expression, which restores the sensitivity of TrkAIII expressing SH-SY5Y cells to Rotenone, Paraquat and LY83583-induced mitochondrial free radical ROS production and ROS-mediated death. The data implicate the novel TrkAIII/SOD2 axis in promoting NB resistance to mitochondrial free radical-mediated death and staminality, and suggest that the combined use of TrkAIII and/or SOD2 inhibitors together with agents that induce mitochondrial free radical ROS-mediated death could provide a therapeutic advantage that may also target the stem cell niche in high TrkA expressing unfavourable NB. PMID:24736663

Regulatory considerations in assessing the potential for Phytophthora ramorum to cause environmental impact to ecozones outside the west coast "fog belt" in North America

Treesearch

John McDonald; Gary Kristjansson; Stephen Miller; Shane Sela

2010-01-01

Sudden oak death (SOD) is a disease caused by Phytophthora ramorum that is characterized by lethal trunk lesions that affect tanoak (Lithocarpus densiflorus), and a few oak species, principally coast live oak (Quercus agrifolia). It was first observed in Marin County, California, in 1994, and now has been...

Effects of diversity, topography, and interannual climate variability on pathogen spillover

Treesearch

Whalen W. Dillon; Ross K. Meentemeyer; David M. Rizzo

2017-01-01

Our knowledge of sudden oak death (SOD) disease dynamics indicate that without bay laurel (Umbellularia californica) there is seldom oak (Quercus) infection. This requirement of an alternate host species for disease transmission to oak species is an example of pathogen spillover. We developed a path analysis to test...

Eukaryotic copper-only superoxide dismutases (SODs): A new class of SOD enzymes and SOD-like protein domains.

PubMed

Robinett, Natalie G; Peterson, Ryan L; Culotta, Valeria C

2018-03-30

The copper-containing superoxide dismutases (SODs) represent a large family of enzymes that participate in the metabolism of reactive oxygen species by disproportionating superoxide anion radical to oxygen and hydrogen peroxide. Catalysis is driven by the redox-active copper ion, and in most cases, SODs also harbor a zinc at the active site that enhances copper catalysis and stabilizes the protein. Such bimetallic Cu,Zn-SODs are widespread, from the periplasm of bacteria to virtually every organelle in the human cell. However, a new class of copper-containing SODs has recently emerged that function without zinc. These copper-only enzymes serve as extracellular SODs in specific bacteria ( i.e. Mycobacteria), throughout the fungal kingdom, and in the fungus-like oomycetes. The eukaryotic copper-only SODs are particularly unique in that they lack an electrostatic loop for substrate guidance and have an unusual open-access copper site, yet they can still react with superoxide at rates limited only by diffusion. Copper-only SOD sequences similar to those seen in fungi and oomycetes are also found in the animal kingdom, but rather than single-domain enzymes, they appear as tandem repeats in large polypeptides we refer to as CSRPs (copper-only SOD-repeat proteins). Here, we compare and contrast the Cu,Zn versus copper-only SODs and discuss the evolution of copper-only SOD protein domains in animals and fungi. © 2018 by The American Society for Biochemistry and Molecular Biology, Inc.

Chemical ecology of sudden oak death/ambrosia beetle interactions

Treesearch

Frances S. Ockels; Pierluigi Bonello; Brice McPherson; David L. Wood

2006-01-01

Coast live oaks, Quercus agrifolia, infected with Phytophthora ramorum in California produce a characteristic sequence of symptoms and signs. Ambrosia beetles consistently tunnel into the bark of bleeding cankers in naturally infected trees. In field monitoring conducted since 2000, every bleeding coast live oak that subsequently...

Sudden oak death-caused changes to surface fuel loading and potential fire behavior in Douglas-fir-tanoak forests

Treesearch

Y.S. Valachovic; C.A. Lee; H. Scanlon; J.M. Varner; R. Glebocki; B.D. Graham; D.M. Rizzo

2011-01-01

We compared stand structure and fuel loading in northwestern California forests invaded by Phytophthora ramorum, the cause of sudden oak death, to assess whether the continued presence of this pathogen alters surface fuel loading and potential fire behavior in ways that may encumber future firefighting response. To attempt to account for these...

Interacting disturbances: Wildfire severity affected by stage of forest disease invasion

Treesearch

Margaret Metz; Kerri Frangioso; Ross Meentemeyer; David Rizzo

2010-01-01

Sudden oak death (SOD) is an emerging forest disease causing extensive tree mortality in coastal California forests. Recent California wildfires provided an opportunity to test a major assumption underlying discussions of SOD and land management: SOD mortality will increase fire severity. We examined pre-fire fuels from host species in a forest monitoring plot network...

Assessment of ligand binding at a site relevant to SOD1 oxidation and aggregation.

PubMed

Manjula, Ramu; Wright, Gareth S A; Strange, Richard W; Padmanabhan, Balasundaram

2018-05-01

Cu/Zn superoxide dismutase-1 (SOD1) mutations are causative for a subset of amyotrophic lateral sclerosis (ALS) cases. These mutations lead to structural instability, aggregation and ultimately motor neuron death. We have determined crystal structures of SOD1 in complex with a naphthalene-catechol-linked compound which binds with low micro-molar affinity to a site important for oxidative damage-induced aggregation. SOD1 Trp32 oxidation is indeed significantly inhibited by ligand binding. Our work shows how compound linking can be applied successfully to ligand interactions on the SOD1 surface to generate relatively good binding strength. The ligand, positioned in a region important for SOD1 fibrillation, offers the possibility that it, or a similar compound, could prevent the abnormal self-association that drives SOD1 toxicity in ALS. © 2018 Federation of European Biochemical Societies.

Size Matters a Lot: Drought-Affected Italian Oaks Are Smaller and Show Lower Growth Prior to Tree Death

PubMed Central

Colangelo, Michele; Camarero, Jesús J.; Borghetti, Marco; Gazol, Antonio; Gentilesca, Tiziana; Ripullone, Francesco

2017-01-01

Hydraulic theory suggests that tall trees are at greater risk of drought-triggered death caused by hydraulic failure than small trees. In addition the drop in growth, observed in several tree species prior to death, is often interpreted as an early-warning signal of impending death. We test these hypotheses by comparing size, growth, and wood-anatomy patterns of living and now-dead trees in two Italian oak forests showing recent mortality episodes. The mortality probability of trees is modeled as a function of recent growth and tree size. Drift-diffusion-jump (DDJ) metrics are used to detect early-warning signals. We found that the tallest trees of the anisohydric Italian oak better survived drought contrary to what was predicted by the theory. Dead trees were characterized by a lower height and radial-growth trend than living trees in both study sites. The growth reduction of now-dead trees started about 10 years prior to their death and after two severe spring droughts during the early 2000s. This critical transition in growth was detected by DDJ metrics in the most affected site. Dead trees were also more sensitive to drought stress in this site indicating different susceptibility to water shortage between trees. Dead trees did not form earlywood vessels with smaller lumen diameter than surviving trees but tended to form wider latewood vessels with a higher percentage of vessel area. Since living and dead trees showed similar competition we did not expect that moderate thinning and a reduction in tree density would increase the short-term survival probability of trees. PMID:28270816

Size Matters a Lot: Drought-Affected Italian Oaks Are Smaller and Show Lower Growth Prior to Tree Death.

PubMed

Colangelo, Michele; Camarero, Jesús J; Borghetti, Marco; Gazol, Antonio; Gentilesca, Tiziana; Ripullone, Francesco

2017-01-01

Hydraulic theory suggests that tall trees are at greater risk of drought-triggered death caused by hydraulic failure than small trees. In addition the drop in growth, observed in several tree species prior to death, is often interpreted as an early-warning signal of impending death. We test these hypotheses by comparing size, growth, and wood-anatomy patterns of living and now-dead trees in two Italian oak forests showing recent mortality episodes. The mortality probability of trees is modeled as a function of recent growth and tree size. Drift-diffusion-jump (DDJ) metrics are used to detect early-warning signals. We found that the tallest trees of the anisohydric Italian oak better survived drought contrary to what was predicted by the theory. Dead trees were characterized by a lower height and radial-growth trend than living trees in both study sites. The growth reduction of now-dead trees started about 10 years prior to their death and after two severe spring droughts during the early 2000s. This critical transition in growth was detected by DDJ metrics in the most affected site. Dead trees were also more sensitive to drought stress in this site indicating different susceptibility to water shortage between trees. Dead trees did not form earlywood vessels with smaller lumen diameter than surviving trees but tended to form wider latewood vessels with a higher percentage of vessel area. Since living and dead trees showed similar competition we did not expect that moderate thinning and a reduction in tree density would increase the short-term survival probability of trees.

The mighty oak faces challenges in the Pacific West

Treesearch

Gail Wells

2010-01-01

In popular imagination, the oak tree stands for strength, endurance, and longevity. But in the coastal lowlands and central valleys of British Columbia, Washington, Oregon, and California, oaks face a battery of natural and human-induced threats. Sudden oak death, caused by a virulent pathogen identified in 2000, has killed millions of tanoaks, California black oaks,...

Lessons Learned from a Decade of Sudden Oak Death in California: Evaluating Local Management

NASA Astrophysics Data System (ADS)

Alexander, Janice; Lee, Christopher A.

2010-09-01

Sudden Oak Death has been impacting California’s coastal forests for more than a decade. In that time, and in the absence of a centrally organized and coordinated set of mandatory management actions for this disease in California’s wildlands and open spaces, many local communities have initiated their own management programs. We present five case studies to explore how local-level management has attempted to control this disease. From these case studies, we glean three lessons: connections count, scale matters, and building capacity is crucial. These lessons may help management, research, and education planning for future pest and disease outbreaks.

Lessons Learned from a Decade of Sudden Oak Death in California: Evaluating Local Management

PubMed Central

Alexander, Janice

2010-01-01

Sudden Oak Death has been impacting California’s coastal forests for more than a decade. In that time, and in the absence of a centrally organized and coordinated set of mandatory management actions for this disease in California’s wildlands and open spaces, many local communities have initiated their own management programs. We present five case studies to explore how local-level management has attempted to control this disease. From these case studies, we glean three lessons: connections count, scale matters, and building capacity is crucial. These lessons may help management, research, and education planning for future pest and disease outbreaks. PMID:20559634

Temporal Epidemiology of Sudden Oak Death in Oregon.

PubMed

Peterson, Ebba K; Hansen, Everett M; Kanaskie, Alan

2015-07-01

An effort to eradicate Phytophthora ramorum, causal agent of sudden oak death, has been underway since its discovery in Oregon forests. Using an information-theoretical approach, we sought to model yearly variation in the size of newly infested areas and dispersal distance. Maximum dispersal distances were best modeled by spring and winter precipitation 2 years before detection, and infestation size the year prior. Infestation size was best modeled by infestation size and spring precipitation the year prior. In our interpretation, there is a 2-year delay between the introduction of inoculum and onset of mortality for a majority of sites. The year-long gap in between allows ample time for the production of inoculum contributing to the spread of P. ramorum. This is supported by epidemic development following changes in eradication protocols precipitated by an outbreak in 2011, attributable to a 2009 treatment delay and an uncharacteristically wet spring in 2010. Posteradication, we have observed an increase in the total area of new outbreaks and increased frequency in dispersal distances greater than 4 km. Although the eradication program has not eliminated P. ramorum from Oregon forests, it has likely moderated this epidemic, emphasizing the need for prompt treatment of future invasive forest pathogens.

Genetic diversity, structure, and demographic change in tanoak, Lithocarpus densiflorus (Fagaceae), the most susceptible species to sudden oak death in California

Treesearch

A. Nettel; R. S. Dodd; Z. Afzal-Rafii

2009-01-01

Knowledge of population genetic structure of tanoak (Lithocarpus densiflorus) is of interest to pathologists seeking natural variation in resistance to sudden oak death disease, to resource managers who need indications of conservation priorities in this species now threatened by the introduced pathogen (Phytophthora ramorum),...

Delayed Disease Onset and Extended Survival in the SOD1G93A Rat Model of Amyotrophic Lateral Sclerosis after Suppression of Mutant SOD1 in the Motor Cortex

PubMed Central

Thomsen, Gretchen M.; Gowing, Genevieve; Latter, Jessica; Chen, Maximus; Vit, Jean-Philippe; Staggenborg, Kevin; Avalos, Pablo; Alkaslasi, Mor; Ferraiuolo, Laura; Likhite, Shibi; Kaspar, Brian K.

2014-01-01

Sporadic amyotrophic lateral sclerosis (ALS) is a fatal disease with unknown etiology, characterized by a progressive loss of motor neurons leading to paralysis and death typically within 3–5 years of onset. Recently, there has been remarkable progress in understanding inherited forms of ALS in which well defined mutations are known to cause the disease. Rodent models in which the superoxide dismutase-1 (SOD1) mutation is overexpressed recapitulate hallmark signs of ALS in patients. Early anatomical changes in mouse models of fALS are seen in the neuromuscular junctions (NMJs) and lower motor neurons, and selective reduction of toxic mutant SOD1 in the spinal cord and muscle of these models has beneficial effects. Therefore, much of ALS research has focused on spinal motor neuron and NMJ aspects of the disease. Here we show that, in the SOD1G93A rat model of ALS, spinal motor neuron loss occurs presymptomatically and before degeneration of ventral root axons and denervation of NMJs. Although overt cell death of corticospinal motor neurons does not occur until disease endpoint, we wanted to establish whether the upper motor neuron might still play a critical role in disease progression. Surprisingly, the knockdown of mutant SOD1 in only the motor cortex of presymptomatic SOD1G93A rats through targeted delivery of AAV9–SOD1–shRNA resulted in a significant delay of disease onset, expansion of lifespan, enhanced survival of spinal motor neurons, and maintenance of NMJs. This datum suggests an early dysfunction and thus an important role of the upper motor neuron in this animal model of ALS and perhaps patients with the disease. PMID:25411487

Delayed disease onset and extended survival in the SOD1G93A rat model of amyotrophic lateral sclerosis after suppression of mutant SOD1 in the motor cortex.

PubMed

Thomsen, Gretchen M; Gowing, Genevieve; Latter, Jessica; Chen, Maximus; Vit, Jean-Philippe; Staggenborg, Kevin; Avalos, Pablo; Alkaslasi, Mor; Ferraiuolo, Laura; Likhite, Shibi; Kaspar, Brian K; Svendsen, Clive N

2014-11-19

Sporadic amyotrophic lateral sclerosis (ALS) is a fatal disease with unknown etiology, characterized by a progressive loss of motor neurons leading to paralysis and death typically within 3-5 years of onset. Recently, there has been remarkable progress in understanding inherited forms of ALS in which well defined mutations are known to cause the disease. Rodent models in which the superoxide dismutase-1 (SOD1) mutation is overexpressed recapitulate hallmark signs of ALS in patients. Early anatomical changes in mouse models of fALS are seen in the neuromuscular junctions (NMJs) and lower motor neurons, and selective reduction of toxic mutant SOD1 in the spinal cord and muscle of these models has beneficial effects. Therefore, much of ALS research has focused on spinal motor neuron and NMJ aspects of the disease. Here we show that, in the SOD1(G93A) rat model of ALS, spinal motor neuron loss occurs presymptomatically and before degeneration of ventral root axons and denervation of NMJs. Although overt cell death of corticospinal motor neurons does not occur until disease endpoint, we wanted to establish whether the upper motor neuron might still play a critical role in disease progression. Surprisingly, the knockdown of mutant SOD1 in only the motor cortex of presymptomatic SOD1(G93A) rats through targeted delivery of AAV9-SOD1-shRNA resulted in a significant delay of disease onset, expansion of lifespan, enhanced survival of spinal motor neurons, and maintenance of NMJs. This datum suggests an early dysfunction and thus an important role of the upper motor neuron in this animal model of ALS and perhaps patients with the disease. Copyright © 2014 the authors 0270-6474/14/3415587-14$15.00/0.

Size matters a lot: tree height and prior growth predict drought-induced tree death in Italian oak forests

NASA Astrophysics Data System (ADS)

Ripullone, F.; Colangelo, M.; Camarero, J. J.; Gazol, A.; Borghetti, M.; Gentilesca, T.

2016-12-01

Climate warming is expected to amplify drought stress resulting in the occurrence of more widespread dieback episodes and increasing mortality rates. This has pushed the search of reliable and robust early-warning indicators of impending drought-triggered tree death. Recent studies highlight how level of defoliation or age of trees strictly coact with drought in leading to forest decline. In addition, tree size and the tree-to-tree competition for water could also contribute to tree death in drought-prone sites. In this regard, it has been predicted that tall trees with isohydric stomatal regulation are most likely to die due to drought stress. Here, we test this hypothesis by analyzing size, age, competition and growth data in a Mediterranean oak species characterized by anisohydric behaviour, showing recent drought-induced mortality in two Italian forest sites. At both study sites, tree height was associated to the probability of dying. However, this association was opposite to published predictions because living trees were taller than dead trees at both sites. Neither age nor competition intensity played significant roles as drivers of tree mortality. Regarding growth data, trends in basal area increment were significantly smaller in dead than in living trees. Differences were most marked at mid (15 years prior to death) than at short (10 years) or long-term (35 year) scales. This is probably not related to intrinsic growth features of the study species but it can be explained because the most severe drought since 1950 occurred in 2000 at the study area, i.e. 15 years prior to the increase of tree mortality and when growth of living and dead trees started diverging. Lastly, we discuss potential factors which may explain why smaller individuals of anisohydric tree species such as Mediterranean oaks are prone to drought-induced tree death.

Caspase 6 has a protective role in SOD1(G93A) transgenic mice.

PubMed

Hogg, Marion C; Mitchem, Mollie R; König, Hans-Georg; Prehn, Jochen H M

2016-06-01

In amyotrophic lateral sclerosis (ALS), it has been suggested that the process of neurodegeneration starts at the neuromuscular junction and is propagated back along axons towards motor neurons. Caspase-dependent pathways are well established as a cause of motor neuron death, and recent work in other disease models indicated a role for caspase 6 in axonal degeneration. Therefore we hypothesised that caspase 6 may be involved in motor neuron death in ALS. To investigate the role of caspase 6 in ALS we profiled protein levels of caspase-6 throughout disease progression in the ALS mouse model SOD1(G93A); this did not reveal differences in caspase 6 levels during disease. To investigate the role of caspase 6 further we generated a colony with SOD1(G93A) transgenic mice lacking caspase 6. Analysis of the transgenic SOD1(G93A); Casp6(-/-) revealed an exacerbated phenotype with motor dysfunction occurring earlier and a significantly shortened lifespan when compared to transgenic SOD1(G93A); Casp6(+/+) mice. Immunofluorescence analysis of the neuromuscular junction revealed no obvious difference between caspase 6(+/+) and caspase 6(-/-) in non-transgenic mice, while the SOD1(G93A) transgenic mice showed severe degeneration compared to non-transgenic mice in both genotypes. Our data indicate that caspase-6 does not exacerbate ALS pathogenesis, but may have a protective role. Copyright © 2016 Elsevier B.V. All rights reserved.

Detection and eradication of Phytophthora ramorum from Oregon Forests, 2001-2008

Treesearch

Alan Kanaskie; Everett Hansen; Ellen Michaels Goheen; Nancy Osterbauer; Michael McWilliams; Jon Laine; Michael Thompson; Stacy Savona; Harvey Timeus; Bill Woosley; Wendy Sutton; Paul Reeser; Rick Shultz; Dan Hilburn

2010-01-01

Sudden oak death (SOD), caused by Phytophthora ramorum, was first discovered in Oregon forests by aerial survey in July 2001. Since then an interagency team has been working with landowners to eradicate the pathogen by cutting and burning all infected and nearby host plants. The Oregon SOD program now consists of the following elements: early...

Mapping hardwood mortality for the early detection of P. ramorum: an assessment of aerial surveys and object-oriented image analysis

Treesearch

Erik Haunreiter; Zhanfeng Liu; Jeff Mai; Zachary Heath; Lisa Fischer

2008-01-01

Effective monitoring and identification of areas of hardwood mortality is a critical component in the management of sudden oak death (SOD). From 2001 to 2005, aerial surveys covering 13.5 million acres in California were conducted to map and monitor hardwood mortality for the early detection of Phytophthora ramorum, the pathogen responsible for SOD....

Ecological evidence of intensive cultivation of oaks by California Indians: implications for the treatment of sudden oak death

Treesearch

Lee Klinger

2006-01-01

The native oaks of California are remarkable for being among the oldest and largest oak trees in the United States besides their great age and size, these trees possess various idiosyncrasies in their arrangements and shapes that appear to defy basic principles of ecology and population biology. When taken together, these and other associated patterns present an...

Phytophthora species in tanoak trees, canopy-drip, soil, and streams in the sudden oak death epidemic area of south-western Oregon, USA

Treesearch

Paul Reeser; Wendy Sutton; Everett Hansen.

2011-01-01

Various Phytophthora species were recovered from tanoak trees, tanoak canopy drip, soils, and streams, which were sampled as part of a larger survey and management effort aimed at limiting the spread of Phytophthora ramorum Werres, De Cock & Man in't Veld (the causal agent of sudden oak death) in an epidemic area...

Consequences of Phytophthora ramorum infection in coast live oaks

Treesearch

Brice McPherson; David L. Wood; Sylvia R. Mori; Pavel Svihra; Richard B. Standiford; N. Maggi. Kelly

2008-01-01

Sudden oak death, caused by Phytophthora ramorum, has infected and killed large numbers of oaks (Quercus spp.) and tanoaks (Lithocarpus densiflorus) in California since the mid 1990s. Since March 2000 we have been investigating the interactions between patterns of disease progression and...

Palmitoylation of superoxide dismutase 1 (SOD1) is increased for familial amyotrophic lateral sclerosis-linked SOD1 mutants.

PubMed

Antinone, Sarah E; Ghadge, Ghanashyam D; Lam, Tukiet T; Wang, Lijun; Roos, Raymond P; Green, William N

2013-07-26

Mutations in Cu,Zn-superoxide dismutase (mtSOD1) cause familial amyotrophic lateral sclerosis (FALS), a neurodegenerative disease resulting from motor neuron degeneration. Here, we demonstrate that wild type SOD1 (wtSOD1) undergoes palmitoylation, a reversible post-translational modification that can regulate protein structure, function, and localization. SOD1 palmitoylation was confirmed by multiple techniques, including acyl-biotin exchange, click chemistry, cysteine mutagenesis, and mass spectrometry. Mass spectrometry and cysteine mutagenesis demonstrated that cysteine residue 6 was the primary site of palmitoylation. The palmitoylation of FALS-linked mtSOD1s (A4V and G93A) was significantly increased relative to that of wtSOD1 expressed in HEK cells and a motor neuron cell line. The palmitoylation of FALS-linked mtSOD1s (G93A and G85R) was also increased relative to that of wtSOD1 when assayed from transgenic mouse spinal cords. We found that the level of SOD1 palmitoylation correlated with the level of membrane-associated SOD1, suggesting a role for palmitoylation in targeting SOD1 to membranes. We further observed that palmitoylation occurred predominantly on disulfide-reduced as opposed to disulfide-bonded SOD1, suggesting that immature SOD1 is the primarily palmitoylated species. Increases in SOD1 disulfide bonding and maturation with increased copper chaperone for SOD1 expression caused a decrease in wtSOD1 palmitoylation. Copper chaperone for SOD1 overexpression decreased A4V palmitoylation less than wtSOD1 and had little effect on G93A mtSOD1 palmitoylation. These findings suggest that SOD1 palmitoylation occurs prior to disulfide bonding during SOD1 maturation and that palmitoylation is increased when disulfide bonding is delayed or decreased as observed for several mtSOD1s.

Predicting potential and actual distribution of sudden oak death in Oregon: prioritizing landscape contexts for early detection and eradication of disease outbreaks

Treesearch

Tomas Vaclavik; Alan Kanaskie; Everett M. Hansen; Janet L. Ohmann; Ross K. Meentemeyer

2010-01-01

An isolated outbreak of the emerging forest disease sudden oak death was discovered in Oregon forests in 2001. Despite considerable control efforts, disease continues to spread from the introduction site due to slow and incomplete detection and eradication. Annual field surveys and laboratory tests between 2001 and 2009 confirmed a total of 802 infested locations. Here...

A Drosophila Model for Amyotrophic Lateral Sclerosis Reveals Motor Neuron Damage by Human SOD1*♦

PubMed Central

Watson, Melanie R.; Lagow, Robert D.; Xu, Kexiang; Zhang, Bing; Bonini, Nancy M.

2008-01-01

Amyotrophic lateral sclerosis (ALS) is a motor neuron disease that leads to loss of motor function and early death. About 5% of cases are inherited, with the majority of identified linkages in the gene encoding copper, zinc-superoxide dismutase (SOD1). Strong evidence indicates that the SOD1 mutations confer dominant toxicity on the protein. To provide new insight into mechanisms of ALS, we have generated and characterized a model for familial ALS in Drosophila with transgenic expression of human SOD1. Expression of wild type or disease-linked (A4V, G85R) mutants of human SOD1 selectively in motor neurons induced progressive climbing deficits. These effects were accompanied by defective neural circuit electrophysiology, focal accumulation of human SOD1 protein in motor neurons, and a stress response in surrounding glia. However, toxicity was not associated with oligomerization of SOD1 and did not lead to neuronal loss. These studies uncover cell-autonomous injury by SOD1 to motor neurons in vivo, as well as non-autonomous effects on glia, and provide the foundation for new insight into injury and protection of motor neurons in ALS. PMID:18596033

Axotomy-induced target disconnection promotes an additional death mechanism involved in motoneuron degeneration in ALS transgenic mice

PubMed Central

Haulcomb, Melissa M.; Mesnard, Nichole A.; Batka, Richard J.; Alexander, Thomas D.; Sanders, Virginia M.; Jones, Kathryn J.

2014-01-01

The target disconnection theory of amyotrophic lateral sclerosis (ALS) pathogenesis suggests disease onset is initiated by a peripheral pathological event resulting in neuromuscular junction loss and motoneuron (MN) degeneration. Pre-symptomatic mSOD1G93A mouse facial MN (FMN) are more susceptible to axotomy-induced cell death than wild-type (WT) FMN, which suggests additional CNS pathology. We have previously determined that the mSOD1 molecular response to facial nerve axotomy is phenotypically regenerative and indistinguishable from WT, whereas the surrounding microenvironment shows significant dysregulation in the mSOD1 facial nucleus. To elucidate the mechanisms underlying the enhanced mSOD1 FMN loss after axotomy, we superimposed the facial nerve axotomy model on pre-symptomatic mSOD1 mice and investigated gene expression for death receptor pathways after target disconnection by axotomy vs. disease progression. We determined that the TNFR1 death receptor pathway is involved in axotomy-induced FMN death in WT, and partially responsible for the mSOD1 FMN death. In contrast, an inherent mSOD1 CNS pathology resulted in a suppressed glial reaction and an upregulation in the Fas death pathway after target disconnection. We propose that the dysregulated mSOD1 glia fail to provide support to injured MN, leading to Fas-induced FMN death. Finally, we demonstrated that during disease progression, the mSOD1 facial nucleus displays target disconnection-induced gene expression changes that mirror those induced by axotomy. This validates the use of axotomy as an investigative tool in understanding the role of peripheral target disconnection in the pathogenesis of ALS. PMID:24424947

Microclimate environmental parameters indexed for Sudden Oak death in Georgia and South Carolina

Treesearch

Pauline Spaine; William J. Otrosina; Stanley J. Zarnoch; Sharon V. Lumpkin

2008-01-01

We monitored Ericaceous habitat in Georgia and South Carolina for temperature, dew point and humidity ranges throughout a two year period. Temperature and humidity data were used to characterize their range in Georgia and South Carolina where potential SOD susceptible hosts occur. This data suggests risk for SOD development may be more widespread in southeastern forest...

HOW to Collect Field Samples and Identify the Oak Wilt Fungus in the Laboratory

Treesearch

Jill Pokorny

1999-01-01

Oak wilt is a serious disease that infects many species of oak. It is responsible for the death of thousands of oak trees in forests, woodlots, and home landscapes each year. Oak wilt occurs in the eastern U.S., in an area delimited by Minnesota, Texas, Pennsylvania, and South Carolina

HoxB2 binds mutant SOD1 and is altered in transgenic model of ALS.

PubMed

Zhai, Jinbin; Lin, Hong; Canete-Soler, Rafaela; Schlaepfer, William W

2005-09-15

Mutations in Cu/Zn superoxide dismutase (SOD1) cause approximately 20% of familial amyotrophic lateral sclerosis by a toxic gain of function; however, the precise mechanisms remain unclear. Here, we report the identification of HoxB2, a homeodomain-containing transcription factor, as a G93A mutant SOD1 interactive protein in a yeast two-hybrid screen. We show that HoxB2 co-precipitates and co-localizes with mutant SOD1 in neuronal cell lines, as well as in brain and spinal cord of G93A mutant SOD1 transgenic mice. Mutagenesis further shows that this interaction is mediated by the central homeodomain of HoxB2. In motor neuron-like NSC-34 cells, overexpression of HoxB2 or its homeodomain decreases the insolubility of mutant SOD1 and inhibits G93A or G86R mutant SOD1-induced neuronal cell death. In human and mouse tissues, we show that expression of HoxB2 persists in adult spinal cord and is primarily localized in nuclei of motor neurons. In G93A transgenic mice, HoxB2 co-localizes with mutant SOD1 and is redistributed to perikarya and proximal neurites of motor neurons. In addition, there is progressive accumulation of HoxB2 and mutant SOD1 as punctate inclusions in the neuropil surrounding motor neurons. Taken together, our findings demonstrate that interaction of HoxB2 with mutant SOD1 occurs in motor neurons of G93A mutant SOD1 transgenic mice and suggest that this interaction may modulate the neurotoxicity of mutant SOD1.

Acylation of Superoxide Dismutase 1 (SOD1) at K122 Governs SOD1-Mediated Inhibition of Mitochondrial Respiration

PubMed Central

Banks, Courtney J.; Rodriguez, Nathan W.; Gashler, Kyle R.; Pandya, Rushika R.; Mortenson, Jeffrey B.; Whited, Matthew D.; Soderblom, Erik J.; Thompson, J. Will; Moseley, M. Arthur; Reddi, Amit R.; Tessem, Jeffery S.; Torres, Matthew P.; Bikman, Benjamin T.

2017-01-01

ABSTRACT In this study, we employed proteomics to identify mechanisms of posttranslational regulation on cell survival signaling proteins. We focused on Cu-Zn superoxide dismutase (SOD1), which protects cells from oxidative stress. We found that acylation of K122 on SOD1, while not impacting SOD1 catalytic activity, suppressed the ability of SOD1 to inhibit mitochondrial metabolism at respiratory complex I. We found that deacylase depletion increased K122 acylation on SOD1, which blocked the suppression of respiration in a K122-dependent manner. In addition, we found that acyl-mimicking mutations at K122 decreased SOD1 accumulation in mitochondria, initially hinting that SOD1 may inhibit respiration directly within the intermembrane space (IMS). However, surprisingly, we found that forcing the K122 acyl mutants into the mitochondria with an IMS-targeting tag did not recover their ability to suppress respiration. Moreover, we found that suppressing or boosting respiration levels toggled SOD1 in or out of the mitochondria, respectively. These findings place SOD1-mediated inhibition of respiration upstream of its mitochondrial localization. Lastly, deletion-rescue experiments show that a respiration-defective mutant of SOD1 is also impaired in its ability to rescue cells from toxicity caused by SOD1 deletion. Together, these data suggest a previously unknown interplay between SOD1 acylation, metabolic regulation, and SOD1-mediated cell survival. PMID:28739857

Redox Regulation of the Superoxide Dismutases SOD3 and SOD2 in the Pulmonary Circulation.

PubMed

Hernandez-Saavedra, Daniel; Swain, Kalin; Tuder, Rubin; Petersen, Steen V; Nozik-Grayck, Eva

2017-01-01

When evaluating the role of redox-regulating signaling in pulmonary vascular diseases, it is intriguing to consider the modulation of key antioxidant enzymes like superoxide dismutase (SOD) because SOD isoforms are regulated by redox reactions, and, in turn, modulate downstream redox sensitive processes. The emerging field of redox biology is built upon understanding the regulation and consequences of tightly controlled and specific reduction-oxidation reactions that are critical for diverse cellular processes including cell signaling. Of relevance, both the site of production of specific reactive oxygen and nitrogen species and the site of the antioxidant defenses are highly compartmentalized within the cell. For example, superoxide is generated during oxidative phosphorylation in the mitochondria as well as by a number of enzymatic sources within the cytosol and at the cell membrane. In the pulmonary circulation, these sources include the mitochondrial electron transport chain, NADPH oxidases (NOX1-4, Duox1,2), nitric oxide synthases, and xanthine oxidase; this important topic has been thoroughly reviewed recently [1]. In parallel with these different cellular sites of superoxide production, the three SOD isoforms are also specifically localized to the cytosol (SOD1), mitochondria (SOD2) or extracellular compartment (SOD3). This chapter focuses on the role of redox mechanisms regulating SOD2 and SOD3, with an emphasis on these processes in the setting of pulmonary hypertension.

Thermal inactivation of infested plants, nursery equipment, and soil is a management option for the treatment of Phytophthora ramorum, causal agent of sudden oak death

Treesearch

Wolfgang Schweigkofler; Vernon Huffman; Karen Suslow; Kathleen Kosta

2017-01-01

Infected nursery plants play an important role in the spread of Phytophthora ramorum , the causal agent of sudden oak death and ramorum blight. In order to minimize the risk for disease transmission to new areas, nurseries are inspected regularly for P. ramorum , and federal regulations require the eradication of...

Rethinking phytophthora—research opportunities and management

Treesearch

Everett Hansen

2008-01-01

It was the second week of June, 2000, the hottest weather on record in San Francisco - hardly Phytophthora weather. But it was that week, at China Camp State Park, that Dave Rizzo and colleagues collected the bark samples from bleeding cankers on coast live oaks that finally moved sudden oak death (SOD) from the “cause unknown” category to “...

Comparing Phytophthora ramorum diagnostic protocols for the national Sudden Oak death stream monitoring program

Treesearch

W. Sutton; E.M. Hansen; P. Reeser; A. Kanaskie

2008-01-01

Oregon was a participant in the pilot test of the national stream monitoring protocol for SOD. We routinely and continuously monitor about 50 streams in and near the SOD quarantine area in southwest Oregon using foliage baits. For the national protocol, we added six additional streams beyond the area of known infestation, and compared results from different diagnostic...

Biomarkers identify coast live oaks that are resistant to the invasive pathogen Phytophthora ramorum

Treesearch

Brice A. McPherson; Sylvia R. Mori; Anna O. Conrad; Stephen Opiyo; Pierluigi Bonello; David L. Wood

2015-01-01

California coast live oaks (Quercus agrifolia) trees have suffered large losses from sudden oak death, caused by the introduced oomycete Phytophthora ramorum. In this review paper, we discuss oak plant chemistry as a potential predictor of disease susceptibility. We have recorded an annual mortality rate of three percent in...

Mutant Copper-Zinc Superoxide Dismutase (SOD1) Induces Protein Secretion Pathway Alterations and Exosome Release in Astrocytes

PubMed Central

Basso, Manuela; Pozzi, Silvia; Tortarolo, Massimo; Fiordaliso, Fabio; Bisighini, Cinzia; Pasetto, Laura; Spaltro, Gabriella; Lidonnici, Dario; Gensano, Francesco; Battaglia, Elisa; Bendotti, Caterina; Bonetto, Valentina

2013-01-01

Amyotrophic lateral sclerosis is the most common motor neuron disease and is still incurable. The mechanisms leading to the selective motor neuron vulnerability are still not known. The interplay between motor neurons and astrocytes is crucial in the outcome of the disease. We show that mutant copper-zinc superoxide dismutase (SOD1) overexpression in primary astrocyte cultures is associated with decreased levels of proteins involved in secretory pathways. This is linked to a general reduction of total secreted proteins, except for specific enrichment in a number of proteins in the media, such as mutant SOD1 and valosin-containing protein (VCP)/p97. Because there was also an increase in exosome release, we can deduce that astrocytes expressing mutant SOD1 activate unconventional secretory pathways, possibly as a protective mechanism. This may help limit the formation of intracellular aggregates and overcome mutant SOD1 toxicity. We also found that astrocyte-derived exosomes efficiently transfer mutant SOD1 to spinal neurons and induce selective motor neuron death. We conclude that the expression of mutant SOD1 has a substantial impact on astrocyte protein secretion pathways, contributing to motor neuron pathology and disease spread. PMID:23592792

The current state of knowledge on operational sanitation measures to lower risk of Phytophthora ramorum spread and the need for further study

Treesearch

Yana Valachovic; Dave Rizzo; Brendan Twieg

2013-01-01

We are working to evaluate risks associated with human spread of the sudden oak death (SOD) pathogen, Phytophthora ramorum, to currently uninfested areas in California. Port-Orford-cedar (Chamaecyparis lawsoniana (A. Murray) Parl.) root disease (POC RD), caused by Phytophthora lateralis, has brought...

Forest succession following wildfire and sudden oak death epidemic

Treesearch

Clay M. DeLong; Kerri M. Frangioso; Margaret R. Metz; Ross K. Meentemeyer; Dave M. Rizzo

2013-01-01

The Big Sur region of central California is a rugged, fire-prone area that has been severely affected by Phytophthora ramorum. Meentemeyer et al. (2008) estimated that over 200,000 oaks and tanoaks had been killed by P. ramorum across the Big Sur ecoregion by 2005. In June of 2008, a complex of lightning-initiated...

Enhanced tethered-flight duration and locomotor activity by overexpression of the human gene SOD1 in Drosophila motorneurons.

PubMed

Petrosyan, Agavni; Hsieh, I-Hui; Phillips, John P; Saberi, Kourosh

2015-03-01

Mutation of the human gene superoxide dismutase (hSOD1) is associated with the fatal neurodegenerative disease familial amyotrophic lateral sclerosis (Lou Gehrig's disease). Selective overexpression of hSOD1 in Drosophila motorneurons increases lifespan to 140% of normal. The current study was designed to determine resistance to lifespan decline and failure of sensorimotor functions by overexpressing hSOD1 in Drosophila's motorneurons. First, we measured the ability to maintain continuous flight and wingbeat frequency (WBF) as a function of age (5 to 50 days). Flies overexpressing hSOD1 under the D42-GAL4 activator were able to sustain flight significantly longer than controls, with the largest effect observed in the middle stages of life. The hSOD1-expressed line also had, on average, slower wingbeat frequencies in late, but not early life relative to age-matched controls. Second, we examined locomotor (exploratory walking) behavior in late life when flies had lost the ability to fly (age ≥ 60 d). hSOD1-expressed flies showed significantly more robust walking activity relative to controls. Findings show patterns of functional decline dissimilar to those reported for other life-extended lines, and suggest that the hSOD1 gene not only delays death but enhances sensorimotor abilities critical to survival even in late life.

Polymorphisms in genes related to oxidative stress (MPO, MnSOD, CAT) and survival after treatment for breast cancer.

PubMed

Ambrosone, Christine B; Ahn, Jiyoung; Singh, Keshav K; Rezaishiraz, Hamed; Furberg, Helena; Sweeney, Carol; Coles, Brian; Trovato, Andrew

2005-02-01

The proximate cause of cancer cell death by radiation therapy and a number of therapeutic agents is through generation of reactive oxygen species, resulting in DNA damage as well as mitochondrial membrane disruption, triggering the apoptotic cascade. Because mitochondrial manganese superoxide dismutase catalyzes conversion of superoxide radicals to H(2)O(2), with catalase neutralizing H(2)O(2) and myeloperoxidase converting H(2)O(2) to highly reactive hypochlorous acid, we hypothesized that gene variants could impact the efficacy of treatment for breast cancer and improve survival. Women who were treated with radiation and/or chemotherapy for incident breast cancer at the Arkansas Cancer Research Center from 1985 to 1996 were identified. DNA was extracted from paraffin-embedded normal tissue (n = 279), and MnSOD, CAT, and MPO genotypes were determined using mass spectrometry. Cox proportional hazards models were adjusted for age, race, stage with node status, and estrogen receptor and progesterone receptor status. Women who were homozygous for MPO G alleles, associated with increased transcription, had better survival (hazard ratio, 0.60; 95% confidence interval, 0.38-0.95; P = 0.03) than those with common alleles. Both CAT TT and MnSOD CC genotypes were associated with nonsignificant reduced hazard of death. When we combined genotypes associated with higher levels of reactive oxygen species for MnSOD and MPO, women with MnSOD CC and MPO GG genotypes had a 3-fold decrease in hazard of death (hazard ratio, 0.33; 95% confidence interval, 0.13-0.80; P = 0.01). These data indicate that gene variants that impact oxidative stress modify prognosis after treatment for breast cancer.

SOD1 Function and Its Implications for Amyotrophic Lateral Sclerosis Pathology: New and Renascent Themes.

PubMed

Bunton-Stasyshyn, Rosie K A; Saccon, Rachele A; Fratta, Pietro; Fisher, Elizabeth M C

2015-10-01

The canonical role of superoxide dismutase 1 (SOD1) is as an antioxidant enzyme protecting the cell from reactive oxygen species toxicity. SOD1 was also the first gene in which mutations were found to be causative for the neurodegenerative disease amyotrophic lateral sclerosis (ALS), more than 20 years ago. ALS is a relentless and incurable mid-life onset disease, which starts with a progressive paralysis and usually leads to death within 3 to 5 years of diagnosis; in the majority of cases, the intellect appears to remain intact while the motor system degenerates. It rapidly became clear that when mutated SOD1 takes on a toxic gain of function in ALS. However, this novel function remains unknown and many cellular systems have been implicated in disease. Now it seems that SOD1 may play a rather larger role in the cell than originally realized, including as a key modulator of glucose signaling (at least so far in yeast) and in RNA binding. Here, we consider some of the new findings for SOD1 in health and disease, which may shed light on how single amino acid changes at sites throughout this protein can cause devastating neurodegeneration in the mammalian motor system. © The Author(s) 2014.

Superoxide Dismutases, SOD1 and SOD2, Play a Distinct Role in the Fat Body during Pupation in Silkworm Bombyx mori

PubMed Central

Nojima, Yosui; Ito, Katsuhiko; Ono, Hiromasa; Nakazato, Takeru; Bono, Hidemasa; Yokoyama, Takeshi; Sato, Ryoichi; Suetsugu, Yoshitaka; Nakamura, Yuki; Yamamoto, Kimiko; Satoh, Jun-ichi; Tabunoki, Hiroko; Fugo, Hajime

2015-01-01

One way that aerobic biological systems counteract the generation of reactive oxygen species (ROS) is with superoxide dismutase proteins SOD1 and SOD2 that metabolize superoxide radicals to molecular oxygen and hydrogen peroxide or scavenge oxygen radicals produced by the extensive oxidation-reduction and electron-transport reactions that occur in mitochondria. We characterized SOD1 and SOD2 of Bombyx mori isolated from the fat body of larvae. Immunological analysis demonstrated the presence of BmSOD1 and BmSOD2 in the silk gland, midgut, fat body, Malpighian tubules, testis and ovary from larvae to adults. We found that BmSOD2 had a unique expression pattern in the fat body through the fifth instar larval developmental stage. The anti-oxidative functions of BmSOD1 and BmSOD2 were assessed by exposing larvae to insecticide rotenone or vasodilator isosorbide dinitrate, which is an ROS generator in BmN4 cells; however, exposure to these compounds had no effect on the expression levels of either BmSOD protein. Next, we investigated the physiological role of BmSOD1 and BmSOD2 under environmental oxidative stress, applied through whole-body UV irradiation and assayed using quantitative RT-PCR, immunoblotting and microarray analysis. The mRNA expression level of both BmSOD1 and BmSOD2 was markedly increased but protein expression level was increased only slightly. To examine the differences in mRNA and protein level due to UV irradiation intensity, we performed microarray analysis. Gene set enrichment analysis revealed that genes in the insulin signaling pathway and PPAR signaling pathway were significantly up-regulated after 6 and 12 hours of UV irradiation. Taken together, the activities of BmSOD1 and BmSOD2 may be related to the response to UV irradiation stress in B. mori. These results suggest that BmSOD1 and BmSOD2 modulate environmental oxidative stress in the cell and have a specific role in fat body of B. mori during pupation. PMID:25714339

Comparison of the recovery of Phytophthora ramorum from tanoak and California bay laurel, and the potential recovery of inoculum in fog

Treesearch

E.K. Peterson; E.M. Hansen; W. Sutton; P.W. Reeser; J.M. Hulbert

2013-01-01

Oregon's sudden oak death (SOD) eradication program has focused its efforts upon the aggressive treatment of tanoak (Notholithocarpus densiflorus (Hook.& Arn.) Manos, Cannon & S.H. Oh) over all other host species in its efforts to control the spread of Phytophthora ramorum. Despite its known importance to the...

Ancestral seed zones and genetic mixture of tanoak

Treesearch

Richard Dodd; Zara Rafii; Wasima Mayer

2010-01-01

Understanding the genetic structure of tanoak (Lithocarpus densiflorus) is necessary to pathologists seeking natural variation in resistance to Phytophthora ramorum, cause of sudden oak death (SOD), and to resource managers who need indications of conservation priorities for this species now threatened by this introduced pathogen. We investigated...

Dynamics of aerial and terrestrial populations of Phytophthora ramorum in a California watershed under different climatic conditions

Treesearch

Catherine A. Eyre; Melina Kozanitas; Matteo Garbelotto

2013-01-01

We present a study of the epidemiology of sudden oak death (SOD) in California within a watershed based on temporally and spatially replicated surveys of symptoms, viability of the pathogen from symptomatic leaves, and genetic analyses using polymorphic SSR markers.Phytophthora ramorum is sensitive to climate; its...

Phytophthora ramorum regulatory program: present, past, and future direction

Treesearch

Prakash Hebbar; Scott Pfister; Stacy Scott; Anthony Man-Son-Hing; Russ Bulluck

2013-01-01

Sudden oak death (SOD), caused by Phytophthora ramorum, is lethal to tanoak (Notholithocarpus densiflorus (Hook. & Arn.) Manos, Cannon & S.H. Oh), and threatens this species throughout its range in Oregon. The disease was first discovered in coastal southwest Oregon forests in July 2001. Since then an interagency team...

Detection and eradication of Phytophthora ramorum from Oregon forests, 2001-2011

Treesearch

Alan Kanaskie; Everett Hansen; Ellen Michaels Goheen; Nancy Osterbauer; Michael McWilliams; Jon Laine; Michael Thompson; Stacy Savona; Harvey Timeus; Bill Woosley; Randall Wiese; Wendy Sutton; Paul Reeser; Joe Hulbert; Rick Shultz; Dan Hilburn

2013-01-01

Sudden oak death (SOD), caused by Phytophthora ramorum, is lethal to tanoak (Notholithocarpus densiflorus (Hook. & Arn.) Manos, Cannon & S.H. Oh), and threatens this species throughout its range in Oregon. The disease was first discovered in coastal southwest Oregon forests in July 2001. Since then an interagency team...

The new Phytophthora ramorum dynamic in Europe: spread to larch

Treesearch

Anna Harris; Joan Webber

2013-01-01

Sudden oak death (SOD), caused by Phytophthora ramorum, is lethal to tanoak (Notholithocarpus densiflorus (Hook. & Arn.) Manos, Cannon & S.H. Oh), and threatens this species throughout its range in Oregon. The disease was first discovered in coastal southwest Oregon forests in July 2001. Since then an interagency team...

An Overview of Phytophthora ramorum in Washington State

Treesearch

Gary A. Chastagner; Katie Coats; Marianne Elliott

2013-01-01

Sudden oak death (SOD), caused by Phytophthora ramorum, is lethal to tanoak (Notholithocarpus densiflorus (Hook. & Arn.) Manos, Cannon & S.H. Oh), and threatens this species throughout its range in Oregon. The disease was first discovered in coastal southwest Oregon forests in July 2001. Since then an interagency team...

Progress of the Phytophthora ramorum eradication programme in south-western Oregon forests, 2001 - 2009

Treesearch

Alan Kanaskie; Everett Hansen; Ellen Michaels Goheen; Nancy Osterbauer; Michael McWilliams; Jon Laine; Michael Thompson; Stacy Savona; Harvey Timeaus; Bill Woosley; Wendy Sutton; Paul Reeser; Rick Schultz; Dan Hilburn

2011-01-01

Sudden Oak Death (SOD) disease caused by Phytophthora ramorum Werres, de Cock & Man in't Veld was first discovered in Oregon forests in July 2001. Since then, an interagency team has been attempting to eradicate the pathogen though a programme of early detection (aerial and ground surveys, stream baiting...

EU2, a Fourth Evolutionary Lineage of Phytophthora ramorum

Treesearch

Kris Van Poucke; Selma Franceschini; Joan Webber; Kurt Heungens; Clive Brasier

2013-01-01

Sudden oak death (SOD), caused by Phytophthora ramorum, is lethal to tanoak (Notholithocarpus densiflorus (Hook. & Arn.) Manos, Cannon & S.H. Oh), and threatens this species throughout its range in Oregon. The disease was first discovered in coastal southwest Oregon forests in July 2001. Since then an interagency team...

Balancing Detection and Eradication for Control of Epidemics: Sudden Oak Death in Mixed-Species Stands

PubMed Central

Ndeffo Mbah, Martial L.; Gilligan, Christopher A.

2010-01-01

Culling of infected individuals is a widely used measure for the control of several plant and animal pathogens but culling first requires detection of often cryptically-infected hosts. In this paper, we address the problem of how to allocate resources between detection and culling when the budget for disease management is limited. The results are generic but we motivate the problem for the control of a botanical epidemic in a natural ecosystem: sudden oak death in mixed evergreen forests in coastal California, in which species composition is generally dominated by a spreader species (bay laurel) and a second host species (coast live oak) that is an epidemiological dead-end in that it does not transmit infection but which is frequently a target for preservation. Using a combination of an epidemiological model for two host species with a common pathogen together with optimal control theory we address the problem of how to balance the allocation of resources for detection and epidemic control in order to preserve both host species in the ecosystem. Contrary to simple expectations our results show that an intermediate level of detection is optimal. Low levels of detection, characteristic of low effort expended on searching and detection of diseased trees, and high detection levels, exemplified by the deployment of large amounts of resources to identify diseased trees, fail to bring the epidemic under control. Importantly, we show that a slight change in the balance between the resources allocated to detection and those allocated to control may lead to drastic inefficiencies in control strategies. The results hold when quarantine is introduced to reduce the ingress of infected material into the region of interest. PMID:20856850

Galactooligosaccharide improves the animal survival and alleviates motor neuron death in SOD1G93A mouse model of amyotrophic lateral sclerosis.

PubMed

Song, L; Gao, Y; Zhang, X; Le, W

2013-08-29

Amyotrophic lateral sclerosis (ALS) is a progressive and devastating neurodegenerative disease caused by selective degeneration and death of motor neurons. So far very limited therapeutic options have emerged to treat this fatal disease. Homocysteine (Hcy) lowering drugs have been suggested to be a palliative therapy of this disease. Folate, Vitamin B12 (VitB12) and Vitamin B6 (VitB6) are important elements involved in the Hcy metabolism and we proposed that medications which could promote the absorption of folate, VitB12 and VitB6 might have benefit for ALS. Galactooligosaccharides (GOS) is a prebiotic which could significantly improve the absorption and syntheses of B Vitamins. To investigate whether GOS could provide neuroprotective effect in ALS, we applied GOS and GOS-rich prebiotic yogurt in SOD1(G93A) mice and assessed their effects on the disease progression of ALS. Our results showed that GOS and prebiotics yogurt administration significantly delayed the disease onset and prolonged the lifespan in SOD1(G93A) mice. Also, these products increased the concentration of folate, VitB12 and reduced the level of Hcy. Moreover, we found that both GOS and prebiotics yogurt attenuated motor neurons loss, improved the atrophy and mitochondrial activity in myocyte. Furthermore, we demonstrated that GOS and GOS-rich prebiotic treatment suppressed the activation of astrocytes and microglia and regulated several inflammatory- and apoptosis-related factors. Our findings suggested that GOS might have therapeutic potential for ALS, and GOS-rich prebiotic yogurt might be considered as a nutritional therapy for this disease. Copyright © 2013 IBRO. All rights reserved.

Metabolite profiling to predict resistance to Phytophthora ramorum in natural populations of coast live oak

Treesearch

A. Conrad; B. Mcpherson; D. Wood; S. Opiyo; S. Mori; P. Bonello

2013-01-01

Sudden oak death, caused by the invasive oomycete pathogen Phytophthora ramorum, continues to shape the dynamics of coastal populations of oak (Quercus spp.) and tanoak (Notholithocarpus densiflorus (Hook. & Arn.) Manos, Cannon & S.H. Oh) in California and tanoak in southwestern Oregon. Over the...

Engineering of a novel tri-functional enzyme with MnSOD, catalase and cell-permeable activities.

PubMed

Luangwattananun, Piriya; Yainoy, Sakda; Eiamphungporn, Warawan; Songtawee, Napat; Bülow, Leif; Ayudhya, Chartchalerm Isarankura Na; Prachayasittikul, Virapong

2016-04-01

Cooperative function of superoxide dismutase (SOD) and catalase (CAT), in protection against oxidative stress, is known to be more effective than the action of either single enzyme. Chemical conjugation of the two enzymes resulted in molecules with higher antioxidant activity and therapeutic efficacy. However, chemical methods holds several drawbacks; e.g., loss of enzymatic activity, low homogeneity, time-consuming, and the need of chemical residues removal. Yet, the conjugated enzymes have never been proven to internalize into target cells. In this study, by employing genetic and protein engineering technologies, we reported designing and production of a bi-functional protein with SOD and CAT activities for the first time. To enable cellular internalization, cell penetrating peptide from HIV-1 Tat (TAT) was incorporated. Co-expression of CAT-MnSOD and MnSOD-TAT fusion genes allowed simultaneous self-assembly of the protein sequences into a large protein complex, which is expected to contained one tetrameric structure of CAT, four tetrameric structures of MnSOD and twelve units of TAT. The protein showed cellular internalization and superior protection against paraquat-induced cell death as compared to either complex bi-functional protein without TAT or to native enzymes fused with TAT. This study not only provided an alternative strategy to produce multifunctional protein complex, but also gained an insight into the development of therapeutic agent against oxidative stress-related conditions. Copyright © 2016 Elsevier B.V. All rights reserved.

S-acylation of SOD1, CCS, and a stable SOD1-CCS heterodimer in human spinal cords from ALS and non-ALS subjects.

PubMed

Antinone, Sarah E; Ghadge, Ghanashyam D; Ostrow, Lyle W; Roos, Raymond P; Green, William N

2017-01-25

Previously, we found that human Cu, Zn-superoxide dismutase (SOD1) is S-acylated (palmitoylated) in vitro and in amyotrophic lateral sclerosis (ALS) mouse models, and that S-acylation increased for ALS-causing SOD1 mutants relative to wild type. Here, we use the acyl resin-assisted capture (acyl-RAC) assay to demonstrate S-acylation of SOD1 in human post-mortem spinal cord homogenates from ALS and non-ALS subjects. Acyl-RAC further revealed that endogenous copper chaperone for SOD1 (CCS) is S-acylated in both human and mouse spinal cords, and in vitro in HEK293 cells. SOD1 and CCS formed a highly stable heterodimer in human spinal cord homogenates that was resistant to dissociation by boiling, denaturants, or reducing agents and was not observed in vitro unless both SOD1 and CCS were overexpressed. Cysteine mutations that attenuate SOD1 maturation prevented the SOD1-CCS heterodimer formation. The degree of S-acylation was highest for SOD1-CCS heterodimers, intermediate for CCS monomers, and lowest for SOD1 monomers. Given that S-acylation facilitates anchoring of soluble proteins to cell membranes, our findings suggest that S-acylation and membrane localization may play an important role in CCS-mediated SOD1 maturation. Furthermore, the highly stable S-acylated SOD1-CCS heterodimer may serve as a long-lived maturation intermediate in human spinal cord.

S-acylation of SOD1, CCS, and a stable SOD1-CCS heterodimer in human spinal cords from ALS and non-ALS subjects

PubMed Central

Antinone, Sarah E.; Ghadge, Ghanashyam D.; Ostrow, Lyle W.; Roos, Raymond P.; Green, William N.

2017-01-01

Previously, we found that human Cu, Zn-superoxide dismutase (SOD1) is S-acylated (palmitoylated) in vitro and in amyotrophic lateral sclerosis (ALS) mouse models, and that S-acylation increased for ALS-causing SOD1 mutants relative to wild type. Here, we use the acyl resin-assisted capture (acyl-RAC) assay to demonstrate S-acylation of SOD1 in human post-mortem spinal cord homogenates from ALS and non-ALS subjects. Acyl-RAC further revealed that endogenous copper chaperone for SOD1 (CCS) is S-acylated in both human and mouse spinal cords, and in vitro in HEK293 cells. SOD1 and CCS formed a highly stable heterodimer in human spinal cord homogenates that was resistant to dissociation by boiling, denaturants, or reducing agents and was not observed in vitro unless both SOD1 and CCS were overexpressed. Cysteine mutations that attenuate SOD1 maturation prevented the SOD1-CCS heterodimer formation. The degree of S-acylation was highest for SOD1-CCS heterodimers, intermediate for CCS monomers, and lowest for SOD1 monomers. Given that S-acylation facilitates anchoring of soluble proteins to cell membranes, our findings suggest that S-acylation and membrane localization may play an important role in CCS-mediated SOD1 maturation. Furthermore, the highly stable S-acylated SOD1-CCS heterodimer may serve as a long-lived maturation intermediate in human spinal cord. PMID:28120938

7 CFR 1437.309 - Turfgrass sod.

Code of Federal Regulations, 2012 CFR

2012-01-01

... sod shall be a square yard. (d) Turfgrass sod having any value shall be considered as worth full value... information to CCC regarding the average number of square yards per acre and all unharvested areas. ...

7 CFR 1437.309 - Turfgrass sod.

Code of Federal Regulations, 2014 CFR

2014-01-01

... sod shall be a square yard. (d) Turfgrass sod having any value shall be considered as worth full value... information to CCC regarding the average number of square yards per acre and all unharvested areas. ...

7 CFR 1437.309 - Turfgrass sod.

Code of Federal Regulations, 2013 CFR

2013-01-01

... sod shall be a square yard. (d) Turfgrass sod having any value shall be considered as worth full value... information to CCC regarding the average number of square yards per acre and all unharvested areas. ...

Collateral damage: fire and Phytophthora ramorum interact to increase mortality in coast redwood

Treesearch

Margaret R. Metz; J. Morgan Varner; Kerri M. Frangioso; Ross K. Meentemeyer; David M. Rizzo

2013-01-01

Invading species can alter ecosystems by impacting the frequency, severity, and consequences of endemic disturbance regimes (Mack and D'Antonio 1998). Phytophthora ramorum, the causal agent of the emergent disease sudden oak death (SOD), is an invasive pathogen causing widespread tree mortality in coastal forests of California and Oregon. In...

Management of foliar infection of Rhododendron by Phytophthora ramorum with film forming polymers and surfactants

Treesearch

Ebba K. Peterson; Eric Larson

2017-01-01

Phytophthora ramorum, causal agent of sudden oak death (SOD) and ramorum leaf blight, remains a persistent problem of regulatory concern within the horticultural industry. Damages to nurseries have been realized as a result of enforced quarantine and sanitation efforts designed to prevent the spread and establishment of this invasive pathogen....

Use of microsatellite markers derived from whole genome sequence data for identifying polymorphism in Phytophthora ramorum

Treesearch

Kelly Ivors; Matteo Garbelotto; Ineke De Vries; Peter Bonants

2006-01-01

Investigating the population genetics of Phytophthora ramorum, the causal agent of sudden oak death (SOD), is critical to understanding the biology and epidemiology of this important phytopathogen. Raw sequence data (445,000 reads) of P. ramorum was provided by the Joint Genome Institute. Our objective was to develop and utilize...

Effects of phosphate treatments on the growth of Phytophthora ramorum in tanoak stems

Treesearch

Alan Kanaskie; Everett Hansen; Wendy Sutton

2006-01-01

In Oregon, tanoak (Lithocarpus densiflorus) is the tree species most susceptible to Phytophthora ramorum, and Sudden Oak Death (SOD) occurs only in forests where tanoak is present. Oregon is attempting to eradicate the pathogen by complete destruction of host plants in and near infested sites. Although the eradication effort has...

Genetic structure of Notholithocarpus densiflorus(Fagaceae) from the species to the local scale: A review of our knowledge for conservation and replanting

Treesearch

Richard S Dodd; Alejandro Nettel; Jessica W. Wright; Zara Afzal-Rafii

2013-01-01

Tanoak, Notholithocarpus densiflorus (Hook. & Arn.) Manos, Cannon & S. H. Oh (Fagaceae), is an important component of mixed-evergreen forests and woodlands in coastal California and Oregon, with incursions into the Sierra Nevada and the Klamath Ranges. Sudden Oak Death (SOD) is causing severe dieback and mortality in tanoak and could...

Monitoring streams and stormwater ponds for early detection of oomycete plant pathogens in western Washington, a citizen science project

Treesearch

Marianne Elliott; Lucy Rollins; Gary Chastagner

2017-01-01

Sudden Oak Death (SOD) is the common name for a disease caused by Phytophthora ramorum (oomycetes), an invasive plant pathogen of regulatory concern. The nursery, timber, forest specialty product, and Christmas tree industries in Washington are at risk because of the spread of P. ramorum within nurseries and from nurseries into...

Rhododendron leaf baiting of coastal California watersheds for Phytophthora

Treesearch

Tyler B. Bourret; Heather K. Mehl; Kamyar Aram; David M. Rizzo

2017-01-01

For more than a decade, the Rizzo lab and collaborators have monitored northern and central coastal California watersheds each spring and early summer for the presence of Phytophthora using submerged Rhododendron leaves as bait. This served as an early detection tool for the sudden oak death (SOD) pathogen, P. ramorum...

Metal-deficient SOD1 in amyotrophic lateral sclerosis.

PubMed

Hilton, James B; White, Anthony R; Crouch, Peter J

2015-05-01

Mutations to the ubiquitous antioxidant enzyme Cu/Zn superoxide dismutase (SOD1) were the first established genetic cause of the fatal, adult-onset neurodegenerative disease amyotrophic lateral sclerosis (ALS). It is widely accepted that these mutations do not cause ALS via a loss of antioxidant function, but elucidating the alternate toxic gain of function has proven to be elusive. Under physiological conditions, SOD1 binds one copper ion and one zinc ion per monomer to form a highly stable and functional homodimer, but there is now ample evidence to indicate aberrant persistence of SOD1 in an intermediate metal-deficient state may contribute to the protein's involvement in ALS. This review briefly discusses some of the data to support a role for metal-deficient SOD1 in the development of ALS and some of the outcomes from drug development studies that have aimed to modify the symptoms of ALS by targeting the metal state of SOD1. The implications for the metal state of SOD1 in cases of sporadic ALS that do not involve mutant SOD1 are also discussed.

Attraction of ambrosia and bark beetles to coast live oaks infected by Phytophthora ramorum

Treesearch

Brice A. McPherson; Nadir Erbilgin; David L. Wood; Pavel Svihra; Andrew J. Storer; Richard B. Standiford

2008-01-01

Sudden oak death, caused by Phytophthora ramorum (Werres, de Cock & Man in?t Veld), has killed thousands of oaks (Quercus spp.) in coastal California forests since the mid-1990s. Bark and ambrosia beetles that normally colonize dead or severely weakened trees selectively tunnel into the bleeding cankers that are the first...

Aerial and ground surveys for mapping the distribution of Phytophthora ramorum in California

Treesearch

Jeffrey A. Mai; Walter Mark; Lisa Fischer; Amy Jirka

2006-01-01

Since 2001, the USDA Forest Service and California Polytechnic State University, San Luis Obispo have been collaborating for early detection and monitoring of the occurrence of Phytophthora ramorum, the pathogen known to cause sudden oak death (SOD). The effort consists of annual aerial surveys to map hardwood mortality in overstory tree species...

Stream Monitoring for Detection of Phytophthora ramorum in Oregon Tanoak Forests

Treesearch

W. Sutton; E. M. Hansen; P. W. Reeser; A. Kanaskie

2009-01-01

Stream monitoring using leaf baits for early detection of Phytophthora ramorum has been an important part of the Oregon Sudden Oak Death (SOD) program since 2002. Sixty-four streams in and near the Oregon quarantine area in the southwest corner of the state were monitored in 2008. Leaves of rhododendron (Rhododendron macrophyllum...

Resilience of diversity-disease risk interactions following wildfire disturbance

Treesearch

Devon A. Gaydos; Krishna Pacifici; Ross K. Meentemeyer; David. M. Rizzo

2017-01-01

The potential for biodiversity to mitigate risk of infectious diseases in ecological communities – known as the diversity-disease risk hypothesis – is fundamental to understanding links between landscape change and environmental health of forests affected by sudden oak death (SOD). Previous research of the Phytophthora ramorum pathosystem...

An emergent disease causes directional changes in forest species composition in coastal California

Treesearch

Margaret Metz; Kerri Frangioso; Allison Wickland; Ross Meentemeyer; David Rizzo

2012-01-01

Non-native forest pathogens can cause dramatic and long-lasting changes to the composition of forests, and these changes may have cascading impacts on community interactions and ecosystem functioning. Phytophthora ramorum, the causal agent of the emergent forest disease sudden oak death (SOD), has a wide host range, but mortality is concentrated in...

Scaling up from greenhouse to field resistance in tanoaks

Treesearch

Katherine J. Hayden; Richard S. Dodd; Catherine Eyre; Matteo Garbelotto; Jessica W. Wright

2013-01-01

Sudden oak death (SOD) has had a devastating impact on tanoaks (Notholithocarpus densiflorus (Hook. & Arn.) Manos, Cannon & S.H. Oh) in California and Oregon. Tanoaks are a key component of the forests in which they are endemic and are one of the few species that are both killed by Phytophthora ramorum and...

Using sigmoidal curve-fitting in a real- time PCR detection assay to determine detection thresholds

Treesearch

Pedro Uribe; Frank N. Martin

2008-01-01

Phytophthora ramorum, the causal agent of sudden oak death (SOD) is a quarantine pathogen that has forced the implementation of extraordinary measures to track and contain the movement of infected nursery stock both within and outside of the three western states of California, Oregon and Washington. Federal guidelines in the United States for...

Non-native Soluble Oligomers of Cu/Zn Superoxide Dismutase (SOD1) Contain a Conformational Epitope Linked to Cytotoxicity in Amyotrophic Lateral Sclerosis (ALS)

PubMed Central

2015-01-01

Soluble misfolded Cu/Zn superoxide dismutase (SOD1) is implicated in motor neuron death in amyotrophic lateral sclerosis (ALS); however, the relative toxicities of the various non-native species formed by SOD1 as it misfolds and aggregates are unknown. Here, we demonstrate that early stages of SOD1 aggregation involve the formation of soluble oligomers that contain an epitope specific to disease-relevant misfolded SOD1; this epitope, recognized by the C4F6 antibody, has been proposed as a marker of toxic species. Formation of potentially toxic oligomers is likely to be exacerbated by an oxidizing cellular environment, as evidenced by increased oligomerization propensity and C4F6 reactivity when oxidative modification by glutathione is present at Cys-111. These findings suggest that soluble non-native SOD1 oligomers, rather than native-like dimers or monomers, share structural similarity to pathogenic misfolded species found in ALS patients and therefore represent potential cytotoxic agents and therapeutic targets in ALS. PMID:24660965

Relationship of the superoxide dismutase genes, sodA and sodB, to the iron uptake (/ital fur/) regulon in /ital Escherichia coli/ K-12

DOE Office of Scientific and Technical Information (OSTI.GOV)

Niederhoffer, E.C.; Naranjo, C.M.; Fee, J.A.

1988-01-01

Expression of sodA, as indicated by MnSod activity is normal in /ital fur/ mutants. This suggests that sodA is not a member of the /ital fur/ regulon and that the putative Fe-binding, regulatory protein of sodA, suggested by Moody and Hassan is not the Fur protein. by contrast, expression of sodB, as indicated by FeSod activity, is completely blocked in /ital fur/ mutants and the effect is restored by transformation with a plasmid having a normal /ital fur/ locus. The observations suggest that Fur, either directly or indirectly, controls SodB biosynthesis. Additional observations are described which indicate that SodB andmore » Fur act together in a complicated fashion to control the biosynthesis of enterobactin. 26 refs., 3 tabs.« less

A High-Throughput Screening Method for Small-Molecule Inhibitors of the Aberrant Mutant SOD1 and Dynein Complex Interaction

PubMed Central

Tang, Xiaohu; Seyb, Kathleen I.; Huang, Mickey; Schuman, Eli R.; Shi, Ping; Zhu, Haining; Glicksman, Marcie A.

2013-01-01

Aberrant protein-protein interactions are attractive drug targets in a variety of neurodegenerative diseases due to the common pathology of accumulation of protein aggregates. In amyotrophic lateral sclerosis, mutations in SOD1 cause the formation of aggregates and inclusions that may sequester other proteins and disrupt cellular processes. It has been demonstrated that mutant SOD1, but not wild-type SOD1, interacts with the axonal transport motor dynein and that this interaction contributes to motor neuron cell death, suggesting that disrupting this interaction may be a potential therapeutic target. However, it can be challenging to configure a high-throughput screening (HTS)–compatible assay to detect inhibitors of a protein-protein interaction. Here we describe the development and challenges of an HTS for small-molecule inhibitors of the mutant SOD1-dynein interaction. We demonstrate that the interaction can be formed by coexpressing the A4V mutant SOD1 and dynein intermediate complex in cells and that this interaction can be disrupted by compounds added to the cell lysates. Finally, we show that some of the compounds identified from a pilot screen to inhibit the protein-protein interaction with this method specifically disrupt the interaction between the dynein complex and mtSOD1 but not the dynein complex itself when applied to live cells. PMID:22140121

ALS-linked mutant SOD1 proteins promote Aβ aggregates in ALS through direct interaction with Aβ.

PubMed

Jang, Ja-Young; Cho, Hyungmin; Park, Hye-Yoon; Rhim, Hyangshuk; Kang, Seongman

2017-11-04

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive degeneration of motor neurons. Aggregation of ALS-linked mutant Cu/Zn superoxide dismutase (SOD1) is a hallmark of a subset of familial ALS (fALS). Recently, intracellular amyloid-β (Aβ) is detected in motor neurons of both sporadic and familial ALS. We have previously shown that intracellular Aβ specifically interacts with G93A, an ALS-linked SOD1 mutant. However, little is known about the pathological and biological effect of this interaction in neurons. In this study, we have demonstrated that the Aβ-binding region is exposed on the SOD1 surface through the conformational changes due to misfolding of SOD1. Interestingly, we found that the intracellular aggregation of Aβ is enhanced through the direct interaction of Aβ with the Aβ-binding region exposed to misfolded SOD1. Ultimately, increased Aβ aggregation by this interaction promotes neuronal cell death. Consistent with this result, Aβ aggregates was three-fold higher in the brains of G93A transgenic mice than those of non Tg. Our study provides the first direct evidence that Aβ, an AD-linked factor, is associated to the pathogenesis of ALS and provides molecular clues to understand common aggregation mechanisms in the pathogenesis of neurodegenerative diseases. Furthermore, it will provide new insights into the development of therapeutic approaches for ALS. Copyright © 2017 Elsevier Inc. All rights reserved.

Reactive oxygen species trigger motoneuron death in non-cell-autonomous models of ALS through activation of c-Abl signaling.

PubMed

Rojas, Fabiola; Gonzalez, David; Cortes, Nicole; Ampuero, Estibaliz; Hernández, Diego E; Fritz, Elsa; Abarzua, Sebastián; Martinez, Alexis; Elorza, Alvaro A; Alvarez, Alejandra; Court, Felipe; van Zundert, Brigitte

2015-01-01

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease in which pathogenesis and death of motor neurons are triggered by non-cell-autonomous mechanisms. We showed earlier that exposing primary rat spinal cord cultures to conditioned media derived from primary mouse astrocyte conditioned media (ACM) that express human SOD1(G93A) (ACM-hSOD1(G93A)) quickly enhances Nav channel-mediated excitability and calcium influx, generates intracellular reactive oxygen species (ROS), and leads to death of motoneurons within days. Here we examined the role of mitochondrial structure and physiology and of the activation of c-Abl, a tyrosine kinase that induces apoptosis. We show that ACM-hSOD1(G93A), but not ACM-hSOD1(WT), increases c-Abl activity in motoneurons, interneurons and glial cells, starting at 60 min; the c-Abl inhibitor STI571 (imatinib) prevents this ACM-hSOD1(G93A)-mediated motoneuron death. Interestingly, similar results were obtained with ACM derived from astrocytes expressing SOD1(G86R) or TDP43(A315T). We further find that co-application of ACM-SOD1(G93A) with blockers of Nav channels (spermidine, mexiletine, or riluzole) or anti-oxidants (Trolox, esculetin, or tiron) effectively prevent c-Abl activation and motoneuron death. In addition, ACM-SOD1(G93A) induces alterations in the morphology of neuronal mitochondria that are related with their membrane depolarization. Finally, we find that blocking the opening of the mitochondrial permeability transition pore with cyclosporine A, or inhibiting mitochondrial calcium uptake with Ru360, reduces ROS production and c-Abl activation. Together, our data point to a sequence of events in which a toxic factor(s) released by ALS-expressing astrocytes rapidly induces hyper-excitability, which in turn increases calcium influx and affects mitochondrial structure and physiology. ROS production, mediated at least in part through mitochondrial alterations, trigger c-Abl signaling and lead to motoneuron death.

Reactive oxygen species trigger motoneuron death in non-cell-autonomous models of ALS through activation of c-Abl signaling

PubMed Central

Rojas, Fabiola; Gonzalez, David; Cortes, Nicole; Ampuero, Estibaliz; Hernández, Diego E.; Fritz, Elsa; Abarzua, Sebastián; Martinez, Alexis; Elorza, Alvaro A.; Alvarez, Alejandra; Court, Felipe; van Zundert, Brigitte

2015-01-01

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease in which pathogenesis and death of motor neurons are triggered by non-cell-autonomous mechanisms. We showed earlier that exposing primary rat spinal cord cultures to conditioned media derived from primary mouse astrocyte conditioned media (ACM) that express human SOD1G93A (ACM-hSOD1G93A) quickly enhances Nav channel-mediated excitability and calcium influx, generates intracellular reactive oxygen species (ROS), and leads to death of motoneurons within days. Here we examined the role of mitochondrial structure and physiology and of the activation of c-Abl, a tyrosine kinase that induces apoptosis. We show that ACM-hSOD1G93A, but not ACM-hSOD1WT, increases c-Abl activity in motoneurons, interneurons and glial cells, starting at 60 min; the c-Abl inhibitor STI571 (imatinib) prevents this ACM-hSOD1G93A-mediated motoneuron death. Interestingly, similar results were obtained with ACM derived from astrocytes expressing SOD1G86R or TDP43A315T. We further find that co-application of ACM-SOD1G93A with blockers of Nav channels (spermidine, mexiletine, or riluzole) or anti-oxidants (Trolox, esculetin, or tiron) effectively prevent c-Abl activation and motoneuron death. In addition, ACM-SOD1G93A induces alterations in the morphology of neuronal mitochondria that are related with their membrane depolarization. Finally, we find that blocking the opening of the mitochondrial permeability transition pore with cyclosporine A, or inhibiting mitochondrial calcium uptake with Ru360, reduces ROS production and c-Abl activation. Together, our data point to a sequence of events in which a toxic factor(s) released by ALS-expressing astrocytes rapidly induces hyper-excitability, which in turn increases calcium influx and affects mitochondrial structure and physiology. ROS production, mediated at least in part through mitochondrial alterations, trigger c-Abl signaling and lead to motoneuron death. PMID:26106294

Relationship between field resistance to Phytophthora ramorum and constitutive phenolic chemistry of coast live oak

Treesearch

A.M. Nagle; B.A. McPherson; D.L. Wood; M. Garbelotto; A.O. Conrad; S. Opiyo; P. Bonello

2012-01-01

Sudden oak death, caused by Phytophthora ramorum, has resulted in high levels of coast live oak (Quercus agrifolia Nee (CLO) mortality. However, some CLO survive in areas with high disease pressure and may thus be resistant. We tested the hypothesis that such field resistant trees contain constitutively higher levels of...

Understanding the disposal and utilization options for Phytophthora ramorum infested wood

Treesearch

John Shelly; Ramnik Singh; Christine Langford; Tad Mason

2006-01-01

Removing trees inflicted with the sudden oak death (SOD) disease is often necessary because of hazard issues or homeowner/landowner desires. An alternative to disposal of this material is to find acceptable uses for this diseased material. A series of studies is being conducted to help understand the risk of spreading the Phytophthora ramorum...

Tanoak: History, ecology and values

Treesearch

Susan Frankel

2013-01-01

To combat sudden oak death (SOD), scientists needed to understand its primary host – tanoak, Notholithocarpus densiflorus (Hook. & Arn.) Manos, Cannon & S. H. Oh (Fagaceae), so research was initiated on its distribution, utilization and natural history. This Madrono Special Issue presents much of what we have learned, over the past 10 years...

Foreward. Tanoak: History, ecology and values.

Treesearch

S.J. Frankel

2013-01-01

To combat sudden oak death (SOD), scientists needed to understand its primary host – tanoak, Notholithocarpus densiflorus (Hook. & Arn.) Manos, Cannon & S. H. Oh (Fagaceae), so research was initiated on its distribution, utilization and natural history. This Madrono Special Issue presents much of what we have learned, over the past 10 years...

Forest treatment strategies for Phytophthora ramorum

Treesearch

Yana Valachovic; Chris Lee; Jack Marshall; Hugh Scanlon

2010-01-01

Although there is no known cure or preventative on a landscape scale for sudden oak death (SOD), the plant disease caused by Phytophthora ramorum, a variety of management options has been tested with the goal of developing an integrated program of treatment for the pathogen. This paper presents a first attempt to gather together individual...

ELISA and ImmunoStrip® for detection of Phytophthora ramorum, P. kernoviae, and other Phytophthora species

Treesearch

Francisco J. Avila; Barbara Schoedel; Z. Gloria Abad; Michael D. Coffey; Cheryl Blomquist

2009-01-01

The goal of this work was to develop improved tools for the detection of Phytophthora ramorum and P. kernoviae for field and the laboratory use. ImmunoStrip® and ELISA were selected as the test formats for development. Presently, the diagnosis of sudden oak death (SOD) in the national survey of P. ramorum ...

Eradication of Phytophthora ramorum in Oregon forests--status after 3 years

Treesearch

Alan Kanaskie; Nancy Osterbauer; Michael McWilliams; Ellen Goheen; Everett Hansen; Wendy Sutton

2006-01-01

Sudden oak death (SOD) was first discovered in Oregon forests in July 2001 near the city of Brookings. Since September 2001 we have been attempting to eradicate the pathogen by cutting and burning all infected host plants and adjacent apparently uninfected plants. Eradication currently is in progress on approximately 42 sites, totaling 72 acres. The majority of sites...

Isolation and characterization of phytotoxins secreted by Phytophthora ramorum

Treesearch

Daniel K. Manter; Rick G. Kelsey; Joseph J. Karchesy

2006-01-01

Most Phythophthora species secrete a variety of small, hydrophilic proteins that induce a hypersensitive-like response to varying degrees in host and non-host plant species. Our research focuses on the potential role of these proteins in the biology and susceptibility of host species to sudden oak death (SOD). In this paper we reported on the...

Eradication of Phytophthora ramorum from Oregon forests: status after 6 years

Treesearch

Alan Kanaskie; Ellen Goheen; Nancy Osterbauer; Mike McWilliams; Everett Hansen; Wendy Sutton

2008-01-01

Sudden oak death (SOD), caused by Phytophthora ramorum, was first discovered in Oregon forests in July 2001. Since then an interagency team has been working with landowners to eradicate the pathogen by cutting and burning all infected and nearby host plants. During the first two years of the eradication effort, all host vegetation within 15 to 30 m...

Examining the strength and possible causes of the relationship between fire history and Sudden Oak Death.

PubMed

Moritz, Max A; Odion, Dennis C

2005-06-01

Fire can be a dominant process in the ecology of forest vegetation and can also affect forest disease dynamics. Little is known about the relationship between fire and an emerging disease epidemic called Sudden Oak Death, which is caused by a new pathogen, Phytophthora ramorum. This disease has spread across a large, fire-prone portion of California, killing great numbers of oaks and tanoaks and infecting most associated woody plants. Suitable hosts cover a much broader geographic range, raising concern over where the disease may spread. To understand the strength and potential sensitivities of a fire-disease relationship, we examined geographic patterns of confirmed P. ramorum infections in relation to past fire history. We found these infections to be extremely rare within the perimeter of any area burned since 1950. This finding is not caused by spatial bias in sampling for the disease, and is robust to variation in host abundance scenarios and to aggregation of closely spaced sampling locations. We therefore investigated known fire-related factors that could result in significantly lower incidence of the disease in relatively recently burned landscapes. Chemical trends in post-fire environments can influence the success of pathogens like P. ramorum, either by increasing plant nutrient stress or by reducing the occurrence of chemicals antagonistic to Phytophthoras. Succession in the absence of fire leads to greater abundance of host species, which will provide increased habitat for P. ramorum; this will also increase intraspecific competition where these trees are abundant, and other density-dependent effects (e.g. shading) can reduce resource allocation to defenses. Despite these findings about a fire-disease relationship, a much deeper understanding is necessary before fire can be actively used as a tool in slowing the epidemic.

Oak wilt

Treesearch

Robert, Jr. Lewis

1989-01-01

Oak wilt, a major disease of oak trees in North America, is caused by a fungus. It infects the sapwood and stops sap flow to the branches, twigs, and leaves. When sap flow is restricted during the growing season, trees wilt and soon die. In addition to killing trees, oak wilt makes it more difficult to export oak logs to other countries. Logs must be free of oak wilt...

Antioxidant-Chemoprevention Diet Ameliorates Late Effects of Total-Body Irradiation and Supplements Radioprotection by MnSOD-Plasmid Liposome Administration

PubMed Central

Epperly, Michael W.; Wang, Hong; Jones, Jeffrey A.; Dixon, Tracy; Montesinos, Carlos A.; Greenberger, Joel S.

2011-01-01

Many acute and chronic effects of ionizing radiation are mediated by reactive oxygen species and reactive nitrogen species, which deplete antioxidant stores, leading to cellular apoptosis, stem cell depletion and accelerated aging. C57BL/6NHsd mice receiving intravenous MnSOD-PL prior to 9.5 Gy total-body irradiation (TBI) show increased survival from the acute hematopoietic syndrome, and males demonstrated improved long-term survival (Epperly et al., Radiat. Res. 170, 437–444, 2008). We evaluated the effect of an antioxidant-chemopreventive diet compared to a regular diet on long-term survival in female mice. Twenty-four hours before the LD50/30 dose of 9.5 Gy TBI, subgroups of mice were injected intravenously with MnSOD-PL (100 μg plasmid DNA in 100 μl of liposomes). Mice on either diet treated with MnSOD-PL showed decreased death after irradiation compared to irradiated mice on the house diet alone (P = 0.031 for the house diet plus MnSOD-PL or 0.015 for antioxidant diet plus MnSOD-PL). The mice on the antioxidant-chemoprevention diet alone or with MnSOD-PL that survived 30 days after irradiation had a significant increase in survival compared to mice on the regular diet (P = 0.04 or 0.01, respectively). In addition, mice treated with MnSOD-PL only and surviving 30 days after radiation also had increased survival compared to those on the regular diet alone (P = 0.02). Survivors of acute ionizing radiation damage have ameliorated life shortening if they are fed an antioxidant-chemopreventive diet. PMID:21466381

Defining SOD1 ALS natural history to guide therapeutic clinical trial design.

PubMed

Bali, Taha; Self, Wade; Liu, Jingxia; Siddique, Teepu; Wang, Leo H; Bird, Thomas D; Ratti, Elena; Atassi, Nazem; Boylan, Kevin B; Glass, Jonathan D; Maragakis, Nicholas J; Caress, James B; McCluskey, Leo F; Appel, Stanley H; Wymer, James P; Gibson, Summer; Zinman, Lorne; Mozaffar, Tahseen; Callaghan, Brian; McVey, April L; Jockel-Balsarotti, Jennifer; Allred, Peggy; Fisher, Elena R; Lopate, Glenn; Pestronk, Alan; Cudkowicz, Merit E; Miller, Timothy M

2017-02-01

Understanding the natural history of familial amyotrophic lateral sclerosis (ALS) caused by SOD1 mutations (ALS SOD1 ) will provide key information for optimising clinical trials in this patient population. To establish an updated natural history of ALS SOD1 . Retrospective cohort study from 15 medical centres in North America evaluated records from 175 patients with ALS with genetically confirmed SOD1 mutations, cared for after the year 2000. Age of onset, survival, ALS Functional Rating Scale (ALS-FRS) scores and respiratory function were analysed. Patients with the A4V (Ala-Val) SOD1 mutation (SOD1 A4V ), the largest mutation population in North America with an aggressive disease progression, were distinguished from other SOD1 mutation patients (SOD1 non-A4V ) for analysis. Mean age of disease onset was 49.7±12.3 years (mean±SD) for all SOD1 patients, with no statistical significance between SOD1 A4V and SOD1 non-A4V (p=0.72, Kruskal-Wallis). Total SOD1 patient median survival was 2.7 years. Mean disease duration for all SOD1 was 4.6±6.0 and 1.4±0.7 years for SOD1 A4V . SOD1 A4V survival probability (median survival 1.2 years) was significantly decreased compared with SOD1 non-A4V (median survival 6.8 years; p<0.0001, log-rank). A statistically significant increase in ALS-FRS decline in SOD1 A4V compared with SOD1 non-A4V participants (p=0.02) was observed, as well as a statistically significant increase in ALS-forced vital capacity decline in SOD1 A4V compared with SOD1 non-A4V (p=0.02). SOD1 A4V is an aggressive, but relatively homogeneous form of ALS. These SOD1-specific ALS natural history data will be important for the design and implementation of clinical trials in the ALS SOD1 patient population. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.

Spatial and Temporal Analysis of Populations of the Sudden Oak Death Pathogen in Oregon Forests.

PubMed

Kamvar, Z N; Larsen, M M; Kanaskie, A M; Hansen, E M; Grünwald, N J

2015-07-01

Sudden oak death caused by the oomycete Phytophthora ramorum was first discovered in California toward the end of the 20th century and subsequently emerged on tanoak forests in Oregon before its first detection in 2001 by aerial surveys. The Oregon Department of Forestry has since monitored the epidemic and sampled symptomatic tanoak trees from 2001 to the present. Populations sampled over this period were genotyped using microsatellites and studied to infer the population genetic history. To date, only the NA1 clonal lineage is established in this region, although three lineages exist on the North American west coast. The original introduction into the Joe Hall area eventually spread to several regions: mostly north but also east and southwest. A new introduction into Hunter Creek appears to correspond to a second introduction not clustering with the early introduction. Our data are best explained by both introductions originating from nursery populations in California or Oregon and resulting from two distinct introduction events. Continued vigilance and eradication of nursery populations of P. ramorum are important to avoid further emergence and potential introduction of other clonal lineages.

Opposite effects of catalase and MnSOD ectopic expression on stress induced defects and mortality in the desmin deficient cardiomyopathy model.

PubMed

Rapti, Kleopatra; Diokmetzidou, Antigoni; Kloukina, Ismini; Milner, Derek J; Varela, Aimilia; Davos, Constantinos H; Capetanaki, Yassemi

2017-09-01

Oxidative stress has been linked strongly to cell death and cardiac remodeling processes, all hallmarks of heart failure. Mice deficient for desmin (des-/-), the major muscle specific intermediate filament protein, develop dilated cardiomyopathy and heart failure characterized by mitochondrial defects and cardiomyocyte death. The cellular and biochemical alterations in the hearts of these mice strongly suggest that oxidative stress is one of the mechanisms contributing to the pathogenesis of the phenotype. Recently, we showed that indeed the desmin deficient cardiomyocytes are under increased oxidative stress. In order to verify these findings in vivo, we generated transgenic animals overexpressing SOD2 (MnSOD) and/or catalase in the heart and crossed them with des-/- mice, thus allowing us to evaluate the contribution of oxidative injury in inherited cardiomyopathies, as well as the therapeutic potential of antioxidant strategies. Moderate MnSOD and/or catalase overexpression in des-/- hearts leads to a marked decrease in intracellular reactive oxygen species (ROS), ameliorates mitochondrial and other ultrastructural defects, minimizes myocardial degeneration and leads to a significant improvement of cardiac function. Importantly, catalase overexpression increased the 50% survival rate of des-/- mice in an obligatory exercise to 100%. In contrast, MnSOD overexpression enhanced the lethality of des-/- mice, underscoring the importance of a fine balanced cellular redox status. Overall, the present study supports the contribution of oxidative stress in the development of des-/- cardiomyopathy and points to a well-considered antioxidant treatment as therapeutic for cardiomyopathies. Copyright © 2017 Elsevier Inc. All rights reserved.

Oak Leaftier and Oak Leafroller (Pest Alert)

Treesearch

USDA Forest Service

1998-01-01

The oak leaftier, Croesia semipurpurana (Kearfott), and the oak leafroller, Archips semiferanus (Walker), are important Tortricidae moths in a complex of native species feeding in the early spring on oak foliage throughout the forests of Eastern North America. Outbreaks periodically develop with frequent and severe defoliation resulting in tree mortality. The last...

ALS-associated mutation SOD1G93A leads to abnormal mitochondrial dynamics in osteocytes.

PubMed

Wang, Huan; Yi, Jianxun; Li, Xuejun; Xiao, Yajuan; Dhakal, Kamal; Zhou, Jingsong

2018-01-01

While the death of motor neuron is a pathological hallmark of amyotrophic lateral sclerosis (ALS), defects in other cell types or organs may also actively contribute to ALS disease progression. ALS patients experience progressive skeletal muscle wasting that may not only exacerbate neuronal degeneration, but likely has a significant impact on bone function. In our previous published study, we have discovered severe bone loss in an ALS mouse model with overexpression of ALS-associated mutation SOD1 G93A (G93A). Here we further provide a mechanistic understanding of the bone loss in ALS animal and cellular models. Combining mitochondrial fluorescent indicators and confocal live cell imaging, we discovered abnormalities in mitochondrial network and dynamics in primary osteocytes derived from the same ALS mouse model G93A. Those mitochondrial defects occur in ALS mice after the onset of neuromuscular symptoms, indicating that mitochondria in bone cells respond to muscle atrophy during ALS disease progression. To examine whether ALS mutation has a direct contribution to mitochondrial dysfunction independent of muscle atrophy, we evaluated mitochondrial morphology and motility in cultured osteocytes (MLO-Y4) with overexpression of mitochondrial targeted SOD1 G93A . Compared with osteocytes overexpressing the wild type SOD1 as a control, the SOD1 G93A osteocytes showed similar defects in mitochondrial network and dynamic as that of the primary osteocytes derived from the ALS mouse model. In addition, we further discovered that overexpression of SOD1 G93A enhanced the expression level of dynamin-related protein 1 (Drp1), a key protein promoting mitochondrial fission activity, and reduced the expression level of optic atrophy protein 1 (OPA1), a key protein related to mitochondrial fusion. A specific mitochondrial fission inhibitor (Mdivi-1) partially reversed the effect of SOD1 G93A on mitochondrial network and dynamics, indicating that SOD1 G93A likely promotes

Compartmentalized oxidative stress in dopaminergic cell death induced by pesticides and complex I inhibitors: Distinct roles of superoxide anion and superoxide dismutases

PubMed Central

Rodriguez-Rocha, Humberto; Garcia-Garcia, Aracely; Pickett, Chillian; Sumin, Li; Jones, Jocelyn; Chen, Han; Webb, Brian; Choi, Jae; Zhou, You; Zimmerman, Matthew C.; Franco, Rodrigo

2013-01-01

The loss of dopaminergic neurons induced by the parkinsonian toxins paraquat, rotenone and 1-methyl-4-phenylpyridinium (MPP+) is associated with oxidative stress. However, controversial reports exist regarding the source/compartmentalization of reactive oxygen species (ROS) generation and its exact role in cell death. We aimed to determine in detail the role of superoxide anion (O2•−), oxidative stress and their subcellular compartmentalization in dopaminergic cell death induced by parkinsonian toxins. Oxidative stress and ROS formation was determined in the cytosol, intermembrane (IMS) and mitochondrial matrix compartments, using dihydroethidine derivatives, the redox sensor roGFP, as well as electron paramagnetic resonance spectroscopy. Paraquat induced an increase in ROS and oxidative stress in both the cytosol and mitochondrial matrix prior to cell death. MPP+ and rotenone primarily induced an increase in ROS and oxidative stress in the mitochondrial matrix. No oxidative stress was detected at the level of the IMS. In contrast to previous studies, overexpression of manganese superoxide dismutase (MnSOD) or copper/zinc SOD (CuZnSOD) had no effect on ROS steady state levels, lipid peroxidation, loss of mitochondrial membrane potential (ΔΨm) and dopaminergic cell death induced by MPP+ or rotenone. In contrast, paraquat-induced oxidative stress and cell death were selectively reduced by MnSOD overexpression, but not by CuZnSOD or manganese-porphyrins. However, MnSOD also failed to prevent ΔΨm loss. Finally, paraquat, but not MPP+ or rotenone, induced the transcriptional activation the redox-sensitive antioxidant response elements (ARE) and nuclear factor kappa-B (NF-κB). These results demonstrate a selective role of mitochondrial O2•− in dopaminergic cell death induced by paraquat, and show that toxicity induced by the complex I inhibitors rotenone and MPP+ does not depend directly on mitochondrial O2•− formation. PMID:23602909

Comparison of Whole Body SOD1 Knockout with Muscle-Specific SOD1 Knockout Mice Reveals a Role for Nerve Redox Signaling in Regulation of Degenerative Pathways in Skeletal Muscle.

PubMed

Sakellariou, Giorgos K; McDonagh, Brian; Porter, Helen; Giakoumaki, Ifigeneia I; Earl, Kate E; Nye, Gareth A; Vasilaki, Aphrodite; Brooks, Susan V; Richardson, Arlan; Van Remmen, Holly; McArdle, Anne; Jackson, Malcolm J

2018-02-01

Lack of Cu,Zn-superoxide dismutase (CuZnSOD) in homozygous knockout mice (Sod1 -/- ) leads to accelerated age-related muscle loss and weakness, but specific deletion of CuZnSOD in skeletal muscle (mSod1KO mice) or neurons (nSod1KO mice) resulted in only mild muscle functional deficits and failed to recapitulate the loss of mass and function observed in Sod1 -/- mice. To dissect any underlying cross-talk between motor neurons and skeletal muscle in the degeneration in Sod1 -/- mice, we characterized neuromuscular changes in the Sod1 -/- model compared with mSod1KO mice and examined degenerative molecular mechanisms and pathways in peripheral nerve and skeletal muscle. In contrast to mSod1KO mice, myofiber atrophy in Sod1 -/- mice was associated with increased muscle oxidative damage, neuromuscular junction degeneration, denervation, nerve demyelination, and upregulation of proteins involved in maintenance of myelin sheaths. Proteomic analyses confirmed increased proteasomal activity and adaptive stress responses in muscle of Sod1 -/- mice that were absent in mSod1KO mice. Peripheral nerve from neither Sod1 -/- nor mSod1KO mice showed increased oxidative damage or molecular responses to increased oxidation compared with wild type mice. Differential cysteine (Cys) labeling revealed a specific redox shift in the catalytic Cys residue of peroxiredoxin 6 (Cys47) in the peripheral nerve from Sod1 -/- mice. Innovation and Conclusion: These findings demonstrate that neuromuscular integrity, redox mechanisms, and pathways are differentially altered in nerve and muscle of Sod1 -/- and mSod1KO mice. Results support the concept that impaired redox signaling, rather than oxidative damage, in peripheral nerve plays a key role in muscle loss in Sod1 -/- mice and potentially sarcopenia during aging. Antioxid. Redox Signal. 28, 275-295.

Mutant SOD1 in cell types other than motor neurons and oligodendrocytes accelerates onset of disease in ALS mice

PubMed Central

Yamanaka, Koji; Boillee, Severine; Roberts, Elizabeth A.; Garcia, Michael L.; McAlonis-Downes, Melissa; Mikse, Oliver R.; Cleveland, Don W.; Goldstein, Lawrence S. B.

2008-01-01

Dominant mutations in ubiquitously expressed superoxide dismutase (SOD1) cause familial ALS by provoking premature death of adult motor neurons. To test whether mutant damage to cell types beyond motor neurons is required for the onset of motor neuron disease, we generated chimeric mice in which all motor neurons and oligodendrocytes expressed mutant SOD1 at a level sufficient to cause fatal, early-onset motor neuron disease when expressed ubiquitously, but did so in a cellular environment containing variable numbers of non-mutant, non-motor neurons. Despite high-level mutant expression within 100% of motor neurons and oligodendrocytes, in most of these chimeras, the presence of WT non-motor neurons substantially delayed onset of motor neuron degeneration, increasing disease-free life by 50%. Disease onset is therefore non-cell autonomous, and mutant SOD1 damage within cell types other than motor neurons and oligodendrocytes is a central contributor to initiation of motor neuron degeneration. PMID:18492803

Oak decline and red oak borer outbreak: impact in upland oak-hickory forests of Arkansas, USA

Treesearch

Laurel J. Haavik; Joshua S. Jones; Larry D. Galligan; James M. Guldin; Fred M. Stephen

2012-01-01

Oak-hickory forests in the Ozark and Ouachita Mountains of Arkansas recently experienced an episode of oak mortality in concert with an outbreak of the red oak borer (Enaphalodes rufulus (Haldeman) (Coleoptera: Cerambycidae)). We utilized data from the Forest Inventory and Analysis (FIA) program of the USDA Forest Service to explore changes in percent red oak (Quercus...

Oak Tree Preservation in Thousand Oaks, California

Treesearch

William F. Elmendorf

1991-01-01

The City of Thousand Oaks over the last 20 years has taken aggressive steps to preserve and protect the City's namesake, the oak tree. First adopted in 1972 as an Emergency City Council Proclamation, the City's Oak Tree Ordinance has been considered by some, to be one of the first and toughest municipal native tree preservation ordinances within the State of...

Defining SOD1 ALS natural history to guide therapeutic clinical trial design

PubMed Central

Bali, Taha; Self, Wade; Liu, Jingxia; Siddique, Teepu; Wang, Leo H; Bird, Thomas D; Ratti, Elena; Atassi, Nazem; Boylan, Kevin B; Glass, Jonathan D; Maragakis, Nicholas J; Caress, James B; McCluskey, Leo F; Appel, Stanley H; Wymer, James P; Gibson, Summer; Zinman, Lorne; Mozaffar, Tahseen; Callaghan, Brian; McVey, April L; Jockel-Balsarotti, Jennifer; Allred, Peggy; Fisher, Elena R; Lopate, Glenn; Pestronk, Alan; Cudkowicz, Merit E; Miller, Timothy M

2016-01-01

Importance Understanding the natural history of familial amyotrophic lateral sclerosis (ALS) caused by SOD1 mutations (ALSSOD1) will provide key information for optimising clinical trials in this patient population. Objective To establish an updated natural history of ALSSOD1. Design, setting and participants Retrospective cohort study from 15 medical centres in North America evaluated records from 175 patients with ALS with genetically confirmed SOD1 mutations, cared for after the year 2000. Main outcomes and measures Age of onset, survival, ALS Functional Rating Scale (ALS-FRS) scores and respiratory function were analysed. Patients with the A4V (Ala-Val) SOD1 mutation (SOD1A4V), the largest mutation population in North America with an aggressive disease progression, were distinguished from other SOD1 mutation patients (SOD1non-A4V) for analysis. Results Mean age of disease onset was 49.7 ±12.3 years (mean±SD) for all SOD1 patients, with no statistical significance between SOD1A4V and SOD1non-A4V (p=0.72, Kruskal-Wallis). Total SOD1 patient median survival was 2.7 years. Mean disease duration for all SOD1 was 4.6±6.0 and 1.4±0.7 years for SOD1A4V. SOD1A4V survival probability (median survival 1.2 years) was significantly decreased compared with SOD1non-A4V (median survival 6.8 years; p<0.0001, log-rank). A statistically significant increase in ALS-FRS decline in SOD1A4V compared with SOD1non-A4V participants (p=0.02) was observed, as well as a statistically significant increase in ALS-forced vital capacity decline in SOD1A4V compared with SOD1non-A4V (p=0.02). Conclusions and relevance SOD1A4V is an aggressive, but relatively homogeneous form of ALS. These SOD1-specific ALS natural history data will be important for the design and implementation of clinical trials in the ALSSOD1 patient population. PMID:27261500

Evaluation of propiconazole operational treatments of oaks for oak wilt control

Treesearch

Jordan Eggers; Jennifer Juzwik; Shawn Bernick; Lori Mordaunt

2005-01-01

Oaks commercially treated with propiconazole on 29 sites in Minnesota in 1998 were evaluated for efficacy in controlling oak wilt. Root graft spread occurred in 39 percent of preventively treated red oaks over 5 years; spread in white oaks occurred only once. Propiconazole generally prevented further disease symptom development in white oaks.

Mortality among workers at Oak Ridge National Laboratory.

PubMed

Richardson, David B; Wing, Steve; Keil, Alexander; Wolf, Susanne

2013-07-01

Workers employed at the Oak Ridge National Laboratory (ORNL) were potentially exposed to a range of chemical and physical hazards, many of which are poorly characterized. We compared the observed deaths among workers to expectations based upon US mortality rates. The cohort included 22,831 workers hired between January 1, 1943 and December 31, 1984. Vital status and cause of death information were ascertained through December 31, 2008. Standardized mortality ratios (SMRs) were computed separately for males and females using US and Tennessee mortality rates; SMRs for men were tabulated separately for monthly-, weekly-, and hourly-paid workers. Hourly-paid males had more deaths due to cancer of the pleura (SMR = 12.09, 95% CI: 4.44, 26.32), cancer of the bladder (SMR = 1.89, 95% CI: 1.26, 2.71), and leukemia (SMR = 1.33, 95% CI: 0.87, 1.93) than expected based on US mortality rates. Female workers also had more deaths than expected from cancer of the bladder (SMR = 2.20, 95% CI: 1.20, 3.69) and leukemia (SMR = 1.64, 95% CI: 1.09, 2.36). The pleural cancer excess has only appeared since the 1980s, approximately 40 years after the start of operations. The bladder cancer excess was larger among workers who also had worked at other Oak Ridge nuclear weapons facilities, while the leukemia excess was among people who had not worked at other DOE facilities. Occupational hazards including asbestos and ionizing radiation may contribute to these excesses. Copyright © 2013 Wiley Periodicals, Inc.

Characteristics of sites and trees affected by rapid white oak mortality as reported by forestry professionals in Missouri

Treesearch

Sharon E. Reed; James T. English; Rose-Marie Muzika; John M. Kabrick; Simeon. Wright

2017-01-01

A new syndrome was named rapid white oak mortality in 2011 to describe the rapid death of white oak trees (Quercus alba L.) within one growing season. A survey with 24 questions about stand and site characteristics, site history, and symptoms was distributed to forestry professionals to gather information about the new syndrome. Sixty-three reports...

RNA interference-mediated silencing of mutant superoxide dismutase rescues cyclosporin A-induced death in cultured neuroblastoma cells

PubMed Central

Maxwell, Michele M.; Pasinelli, Piera; Kazantsev, Aleksey G.; Brown, Robert H.

2004-01-01

Amyotrophic lateral sclerosis (ALS) is a progressive and fatal neurodegenerative disorder resulting from selective death of motor neurons in the brain and spinal cord. In ≈25% of familial ALS cases, the disease is caused by dominantly acting point mutations in the gene encoding cytosolic Cu,Zn superoxide dismutase (SOD1). In cell culture and in rodent models of ALS, mutant SOD1 proteins exhibit dose-dependent toxicity; thus, agents that reduce mutant protein expression would be powerful therapeutic tools. A wealth of recent evidence has demonstrated that the mechanism of RNA-mediated interference (RNAi) can be exploited to achieve potent and specific gene silencing in vitro and in vivo. We have evaluated the utility of RNAi for selective silencing of mutant SOD1 expression in cultured cells and have identified small interfering RNAs capable of specifically inhibiting expression of ALS-linked mutant, but not wild-type, SOD1. We have investigated the functional effects of RNAi-mediated silencing of mutant SOD1 in cultured murine neuroblastoma cells. In this model, stable expression of mutant, but not wild-type, human SOD1 sensitizes cells to cytotoxic stimuli. We find that silencing of mutant SOD1 protects these cells against cyclosporin A-induced cell death. These results demonstrate a positive physiological effect caused by RNAi-mediated silencing of a dominant disease allele. The present study further supports the therapeutic potential of RNAi-based methods for the treatment of inherited human diseases, including ALS. PMID:14981234

Targeting SOD1 induces synthetic lethal killing in BLM- and CHEK2-deficient colorectal cancer cells

PubMed Central

Sajesh, Babu V.; McManus, Kirk J.

2015-01-01

Cancer is a major cause of death throughout the world, and there is a large need for better and more personalized approaches to combat the disease. Over the past decade, synthetic lethal approaches have been developed that are designed to exploit the aberrant molecular origins (i.e. defective genes) that underlie tumorigenesis. BLM and CHEK2 are two evolutionarily conserved genes that are somatically altered in a number of tumor types. Both proteins normally function in preserving genome stability through facilitating the accurate repair of DNA double strand breaks. Thus, uncovering synthetic lethal interactors of BLM and CHEK2 will identify novel candidate drug targets and lead chemical compounds. Here we identify an evolutionarily conserved synthetic lethal interaction between SOD1 and both BLM and CHEK2 in two distinct cell models. Using quantitative imaging microscopy, real-time cellular analyses, colony formation and tumor spheroid models we show that SOD1 silencing and inhibition (ATTM and LCS-1 treatments), or the induction of reactive oxygen species (2ME2 treatment) induces selective killing within BLM- and CHEK2-deficient cells relative to controls. We further show that increases in reactive oxygen species follow SOD1 silencing and inhibition that are associated with the persistence of DNA double strand breaks, and increases in apoptosis. Collectively, these data identify SOD1 as a novel candidate drug target in BLM and CHEK2 cancer contexts, and further suggest that 2ME2, ATTM and LCS-1 are lead therapeutic compounds warranting further pre-clinical study. PMID:26318585

Targeting SOD1 induces synthetic lethal killing in BLM- and CHEK2-deficient colorectal cancer cells.

PubMed

Sajesh, Babu V; McManus, Kirk J

2015-09-29

Cancer is a major cause of death throughout the world, and there is a large need for better and more personalized approaches to combat the disease. Over the past decade, synthetic lethal approaches have been developed that are designed to exploit the aberrant molecular origins (i.e. defective genes) that underlie tumorigenesis. BLM and CHEK2 are two evolutionarily conserved genes that are somatically altered in a number of tumor types. Both proteins normally function in preserving genome stability through facilitating the accurate repair of DNA double strand breaks. Thus, uncovering synthetic lethal interactors of BLM and CHEK2 will identify novel candidate drug targets and lead chemical compounds. Here we identify an evolutionarily conserved synthetic lethal interaction between SOD1 and both BLM and CHEK2 in two distinct cell models. Using quantitative imaging microscopy, real-time cellular analyses, colony formation and tumor spheroid models we show that SOD1 silencing and inhibition (ATTM and LCS-1 treatments), or the induction of reactive oxygen species (2ME2 treatment) induces selective killing within BLM- and CHEK2-deficient cells relative to controls. We further show that increases in reactive oxygen species follow SOD1 silencing and inhibition that are associated with the persistence of DNA double strand breaks, and increases in apoptosis. Collectively, these data identify SOD1 as a novel candidate drug target in BLM and CHEK2 cancer contexts, and further suggest that 2ME2, ATTM and LCS-1 are lead therapeutic compounds warranting further pre-clinical study.

Fire effects on Gambel oak in southwestern ponderosa pine-oak forests

Treesearch

Scott R. Abella; Peter Z. Fulé

2008-01-01

Gambel oak (Quercus gambelii) is ecologically and aesthetically valuable in southwestern ponderosa pine (Pinus ponderosa) forests. Fire effects on Gambel oak are important because fire may be used in pine-oak forests to manage oak directly or to accomplish other management objectives. We used published literature to: (1) ascertain...

Clitocybe tabescens associated with decline and death of Chinese elm and water oak

Treesearch

T. H. Filer; F. I. McCracken

1969-01-01

In 1964, decline symptoms were found on 48 Chinese elms (Ulmus parvifolia) and 2 water oaks (Quercus nigra) in Washington County, Mississippi. Some of their foliage was yellowish, and small lateral branches were dying in parts of the crowns. Large branches later died and the entire crowns were infected.

Two novel cyanobacterial bioluminescent whole-cell bioreporters based on superoxide dismutases MnSod and FeSod to detect superoxide anion.

PubMed

Hurtado-Gallego, J; Martín-Betancor, K; Rodea-Palomares, I; Leganés, F; Rosal, R; Fernández-Piñas, F

2018-06-01

This work describes the construction of two novel self-luminescent bioreporter strains of the cyanobacterium Nostoc sp. PCC 7120 by fusing the promoter region of the sodA and sodB genes (encoding the superoxide dismutases MnSod and FeSod, respectively) to luxCDABE from Photorhabdus luminescens aimed at detecting pollutants that generate reactive oxygen species (ROS), particularly O 2 - . Bioreporters were tested against methyl viologen (MV) as the inducer of superoxide anion (O 2 - ). Both bioreporters were specific for O 2 - and Limits of detection (LODs) and Maximum Permissive Concentrations (MPCs) were calculated: Nostoc sp. PCC 7120 pBG2154 (sodA) had a range of detection from 400 to 1000 pM of MV and for Nostoc sp. PCC 7120 pBG2165 (sodB) the range of detection was from 500 to 1800 pM of MV after 5 h-exposure. To further validate the bioreporters, they were tested with the emerging pollutant Triclosan which induced bioluminescence in both strains. Furthermore, the bioreporters performance was tested in two real environmental samples with different water matrix complexity, spiked with MV. Both bioreporters were induced by O 2 - in these environmental samples. In the case of the river water sample, the amount of bioavailable MV as calculated from the bioreporters output was similar to that nominally added. For the waste water sample, the bioavailable MV concentration detected by the bioreporters was one order of magnitude lower than nominal. These differences could be due to MV complexation with organic matter and/or co-occurring organic contaminants. These results confirm their high sensitivity to O 2 - and their suitability to detect oxidative stress-generating pollutants in fresh-waters. Copyright © 2018 Elsevier Ltd. All rights reserved.

In-vivo effects of knocking-down metabotropic glutamate receptor 5 in the SOD1G93A mouse model of amyotrophic lateral sclerosis.

PubMed

Bonifacino, Tiziana; Cattaneo, Luca; Gallia, Elena; Puliti, Aldamaria; Melone, Marcello; Provenzano, Francesca; Bossi, Simone; Musante, Ilaria; Usai, Cesare; Conti, Fiorenzo; Bonanno, Giambattista; Milanese, Marco

2017-09-01

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder due to loss of upper and lower motor neurons (MNs). The mechanisms of neuronal death are largely unknown, thus prejudicing the successful pharmacological treatment. One major cause for MN degeneration in ALS is represented by glutamate(Glu)-mediated excitotoxicity. We have previously reported that activation of Group I metabotropic Glu receptors (mGluR1 and mGluR5) at glutamatergic spinal cord nerve terminals produces abnormal Glu release in the widely studied SOD1 G93A mouse model of ALS. We also demonstrated that halving mGluR1 expression in the SOD1 G93A mouse had a positive impact on survival, disease onset, disease progression, and on a number of cellular and biochemical readouts of ALS. We generated here SOD1 G93A mice with reduced expression of mGluR5 (SOD1 G93A Grm5 -/+ ) by crossing the SOD1 G93A mutant mouse with the mGluR5 heterozigous Grm5 -/+ mouse. SOD1 G93A Grm5 -/+ mice showed prolonged survival probability and delayed pathology onset. These effects were associated to enhanced number of preserved MNs, decreased astrocyte and microglia activation, reduced cytosolic free Ca 2+ concentration, and regularization of abnormal Glu release in the spinal cord of SOD1 G93A Grm5 -/+ mice. Unexpectedly, only male SOD1 G93A Grm5 -/+ mice showed improved motor skills during disease progression vs. SOD1 G93A mice, while SOD1 G93A Grm5 -/+ females did not. These results demonstrate that a lower constitutive level of mGluR5 has a significant positive impact in mice with ALS and support the idea that blocking Group I mGluRs may represent a potentially effective pharmacological approach to the disease. Copyright © 2017 Elsevier Ltd. All rights reserved.

Oak Symposium Proceedings

Treesearch

Northeastern Forest Experiment Station

1971-01-01

As "tall oaks from little acorns grow", the germ of an idea blossomed into this symposium on the five upland oaks. Called simply the "Oak Symposium", that's what it's all about - a meeting to bring together a summation of the advances made on the silviculture, management, and utilization of the upland oaks. Part of this process is the...

Solid-state NMR studies of metal-free SOD1 fibrillar structures.

PubMed

Banci, Lucia; Blaževitš, Olga; Cantini, Francesca; Danielsson, Jens; Lang, Lisa; Luchinat, Claudio; Mao, Jiafei; Oliveberg, Mikael; Ravera, Enrico

2014-06-01

Copper-zinc superoxide dismutase 1 (SOD1) is present in the protein aggregates deposited in motor neurons of amyotrophic lateral sclerosis (ALS) patients. ALS is a neurodegenerative disease that can be either sporadic (ca. 90%) or familial (fALS). The most widely studied forms of fALS are caused by mutations in the sequence of SOD1. Ex mortuo SOD1 aggregates are usually found to be amorphous. In vitro SOD1, in its immature reduced and apo state, forms fibrillar aggregates. Previous literature data have suggested that a monomeric SOD1 construct, lacking loops IV and VII, (apoSODΔIV-VII), shares the same fibrillization properties of apoSOD1, both proteins having the common structural feature of the central β-barrel. In this work, we show that structural information can be obtained at a site-specific level from solid-state NMR. The residues that are sequentially assignable are found to be located at the putative nucleation site for fibrillar species formation in apoSOD, as detected by other experimental techniques.

Using reinforced native grass sod for biostrips, bioswales, and sediment control.

DOT National Transportation Integrated Search

2008-12-01

The objective of this research was to develop and demonstrate native grass sod for sediment control from disturbed lands associated with California highways. The research evaluated native grass species for inclusion in sod and evaluated the sod at a ...

Conversion of an oak seed orchard to oak silvopasture

Treesearch

K. Connor; L. Dimov; R. Barlow; M. Smith; E. Kirkland

2013-01-01

The potential of hardwood silvopasture has yet to be realized in the Southeastern United States. The decommissioning of the Stauffer Nursery, Opelika, AL, provided the opportunity to intensively research hardwood silvopasture using various oak species. Average crown diameter ranged from 5.9 feet in white oak (Quercus alba) to 10.7 feet in Nuttall oak...

Identification of compounds protective against G93A-SOD1 toxicity for the treatment of amyotrophic lateral sclerosis.

PubMed

Benmohamed, Radhia; Arvanites, Anthony C; Kim, Jinho; Ferrante, Robert J; Silverman, Richard B; Morimoto, Richard I; Kirsch, Donald R

2011-03-01

The underlying cause of amyotrophic lateral sclerosis (ALS), a progressive neurodegenerative disorder, remains unknown. However, there is strong evidence that one pathophysiological mechanism, toxic protein misfolding and/or aggregation, may trigger motor neuron dysfunction and loss. Since the clinical and pathological features of sporadic and familial ALS are indistinguishable, all forms of the disease may be better understood and ultimately treated by studying pathogenesis and therapy in models expressing mutant forms of SOD1. We developed a cellular model in which cell death depended on the expression of G93A-SOD1, a mutant form of superoxide dismutase found in familial ALS patients that produces toxic protein aggregates. This cellular model was optimized for high throughput screening to identify protective compounds from a >50,000 member chemical library. Three novel chemical scaffolds were selected for further study following screen implementation, counter-screening and secondary testing, including studies with purchased analogs. All three scaffolds blocked SOD1 aggregation in high content screening assays and data on the optimization and further characterization of these compounds will be reported separately. These data suggest that optimization of these chemicals scaffolds may produce therapeutic candidates for ALS patients.

Oak wilt: a potential threat to southern and western oak forests

Treesearch

A. Dan Wilson

2001-01-01

Oak wilt is recognized as one of the most destructive diseases to afflict oak species in the United States. The distribution and development of oak wilt in our eastern and midwestern oak forests has been closely linked to changes in forest stand composition, forest management practices, and pathogen dissemination facilitated by human and vector activity. The potential...

Oak Wilt

Treesearch

Charles O. Rexrode; Daniel Brown

1983-01-01

Oak wilt, caused by the fungus Ceratocystis fagacearum (Bretz) Hunt, kills oak trees. It has been found in 21 States, with considerable damage occurring in the Midwest. It was first recognized as an important disease in 1944 in Wisconsin where, in localized areas (less than 100 acres (40.4 ha)), over half the oaks have been killed. Surveys in eight Wisconsin counties...

Is SOD1 loss of function involved in amyotrophic lateral sclerosis?

PubMed Central

Saccon, Rachele A.; Bunton-Stasyshyn, Rosie K. A.; Fisher, Elizabeth M.C.; Fratta, Pietro

2013-01-01

Mutations in the gene superoxide dismutase 1 (SOD1) are causative for familial forms of the neurodegenerative disease amyotrophic lateral sclerosis. When the first SOD1 mutations were identified they were postulated to give rise to amyotrophic lateral sclerosis through a loss of function mechanism, but experimental data soon showed that the disease arises from a—still unknown—toxic gain of function, and the possibility that loss of function plays a role in amyotrophic lateral sclerosis pathogenesis was abandoned. Although loss of function is not causative for amyotrophic lateral sclerosis, here we re-examine two decades of evidence regarding whether loss of function may play a modifying role in SOD1–amyotrophic lateral sclerosis. From analysing published data from patients with SOD1–amyotrophic lateral sclerosis, we find a marked loss of SOD1 enzyme activity arising from almost all mutations. We continue to examine functional data from all Sod1 knockout mice and we find obvious detrimental effects within the nervous system with, interestingly, some specificity for the motor system. Here, we bring together historical and recent experimental findings to conclude that there is a possibility that SOD1 loss of function may play a modifying role in amyotrophic lateral sclerosis. This likelihood has implications for some current therapies aimed at knocking down the level of mutant protein in patients with SOD1–amyotrophic lateral sclerosis. Finally, the wide-ranging phenotypes that result from loss of function indicate that SOD1 gene sequences should be screened in diseases other than amyotrophic lateral sclerosis. PMID:23687121

Gene expression changes in spinal motoneurons of the SOD1(G93A) transgenic model for ALS after treatment with G-CSF.

PubMed

Henriques, Alexandre; Kastner, Stefan; Chatzikonstantinou, Eva; Pitzer, Claudia; Plaas, Christian; Kirsch, Friederike; Wafzig, Oliver; Krüger, Carola; Spoelgen, Robert; Gonzalez De Aguilar, Jose-Luis; Gretz, Norbert; Schneider, Armin

2014-01-01

Amyotrophic lateral sclerosis (ALS) is an incurable fatal motoneuron disease with a lifetime risk of approximately 1:400. It is characterized by progressive weakness, muscle wasting, and death ensuing 3-5 years after diagnosis. Granulocyte-colony stimulating factor (G-CSF) is a drug candidate for ALS, with evidence for efficacy from animal studies and interesting data from pilot clinical trials. To gain insight into the disease mechanisms and mode of action of G-CSF, we performed gene expression profiling on isolated lumbar motoneurons from SOD1(G93A) mice, the most frequently studied animal model for ALS, with and without G-CSF treatment. Motoneurons from SOD1(G93A) mice present a distinct gene expression profile in comparison to controls already at an early disease stage (11 weeks of age), when treatment was initiated. The degree of deregulation increases at a time where motor symptoms are obvious (15 weeks of age). Upon G-CSF treatment, transcriptomic deregulations of SOD1(G93A) motoneurons were notably restored. Discriminant analysis revealed that SOD1 mice treated with G-CSF has a transcriptom close to presymptomatic SOD1 mice or wild type mice. Some interesting genes modulated by G-CSF treatment relate to neuromuscular function such as CCR4-NOT or Prss12. Our data suggest that G-CSF is able to re-adjust gene expression in symptomatic SOD1(G93A) motoneurons. This provides further arguments for G-CSF as a promising drug candidate for ALS.

Gene expression changes in spinal motoneurons of the SOD1G93A transgenic model for ALS after treatment with G-CSF

PubMed Central

Henriques, Alexandre; Kastner, Stefan; Chatzikonstantinou, Eva; Pitzer, Claudia; Plaas, Christian; Kirsch, Friederike; Wafzig, Oliver; Krüger, Carola; Spoelgen, Robert; Gonzalez De Aguilar, Jose-Luis; Gretz, Norbert; Schneider, Armin

2015-01-01

Background: Amyotrophic lateral sclerosis (ALS) is an incurable fatal motoneuron disease with a lifetime risk of approximately 1:400. It is characterized by progressive weakness, muscle wasting, and death ensuing 3–5 years after diagnosis. Granulocyte-colony stimulating factor (G-CSF) is a drug candidate for ALS, with evidence for efficacy from animal studies and interesting data from pilot clinical trials. To gain insight into the disease mechanisms and mode of action of G-CSF, we performed gene expression profiling on isolated lumbar motoneurons from SOD1G93A mice, the most frequently studied animal model for ALS, with and without G-CSF treatment. Results: Motoneurons from SOD1G93A mice present a distinct gene expression profile in comparison to controls already at an early disease stage (11 weeks of age), when treatment was initiated. The degree of deregulation increases at a time where motor symptoms are obvious (15 weeks of age). Upon G-CSF treatment, transcriptomic deregulations of SOD1G93A motoneurons were notably restored. Discriminant analysis revealed that SOD1 mice treated with G-CSF has a transcriptom close to presymptomatic SOD1 mice or wild type mice. Some interesting genes modulated by G-CSF treatment relate to neuromuscular function such as CCR4-NOT or Prss12. Conclusions: Our data suggest that G-CSF is able to re-adjust gene expression in symptomatic SOD1G93A motoneurons. This provides further arguments for G-CSF as a promising drug candidate for ALS. PMID:25653590

Variation in flood tolerance of container-grown seedlings of swamp white oak, bur oak, and white oak

Treesearch

Michael P. Walsh; J.W. Van Sambeek; Mark V. Coggeshall

2008-01-01

How much variation in flood tolerance exists among seedlings within oak species, given the flood frequency of sites from which acorns are collected, has been largely unexplored. Our studies examined initial growth and flood tolerance for seedlings of swamp white oak (Quercus bicolor Willd.), bur oak (Q. macrocarpa L.), and white...

Mortality and community changes drive sudden oak death impacts on litterfall and soil nitrogen cycling.

PubMed

Cobb, Richard C; Eviner, Valerie T; Rizzo, David M

2013-10-01

Few studies have quantified pathogen impacts to ecosystem processes, despite the fact that pathogens cause or contribute to regional-scale tree mortality. We measured litterfall mass, litterfall chemistry, and soil nitrogen (N) cycling associated with multiple hosts along a gradient of mortality caused by Phytophthora ramorum, the cause of sudden oak death. In redwood forests, the epidemiological and ecological characteristics of the major overstory species determine disease patterns and the magnitude and nature of ecosystem change. Bay laurel (Umbellularia californica) has high litterfall N (0.992%), greater soil extractable NO3 -N, and transmits infection without suffering mortality. Tanoak (Notholithocarpus densiflorus) has moderate litterfall N (0.723%) and transmits infection while suffering extensive mortality that leads to higher extractable soil NO3 -N. Redwood (Sequoia sempervirens) has relatively low litterfall N (0.519%), does not suffer mortality or transmit the pathogen, but dominates forest biomass. The strongest impact of pathogen-caused mortality was the potential shift in species composition, which will alter litterfall chemistry, patterns and dynamics of litterfall mass, and increase soil NO3 -N availability. Patterns of P. ramorum spread and consequent mortality are closely associated with bay laurel abundances, suggesting this species will drive both disease emergence and subsequent ecosystem function. © 2013 The Authors. New Phytologist © 2013 New Phytologist Trust.

Oak Growth and Response to Thinning

Treesearch

Stephen R. Shifley

2004-01-01

Oak growth and yield is simultaneously influenced by tree-, stand-, and landscape-scale factors. At the tree scale oak diameter growth varies by tree species (typically n. red oak >= scarlet oak > black oak > white oak > chestnut oak > chinkapin oak > post oak), but oak diameter growth is even more strongly influenced by crown class. Oak stands go...

Oak mortality associated with crown dieback and oak borer attack in the Ozark Highlands

Treesearch

Zhaofei Fan; John M. Kabrick; Martin A. Spetich; Stephen R. Shifley; Randy G. Jensen

2008-01-01

Oak decline and related mortality have periodically plagued upland oak-hickory forests, particularly oak species in the red oak group, across the Ozark Highlands of Missouri, Arkansas and Oklahoma since the late 1970s. Advanced tree age and periodic drought, as well as Armillaria root fungi and oak borer attack are believed to contribute to oak decline and mortality....

Oak mortality associated with crown dieback and oak borer attack in the Ozark Highlands

Treesearch

Zhaofei Fan; John M. Kabrick; Martin A. Spetich; Stephen R. Shifley; Randy G. Jensen

2008-01-01

Oak decline and related mortality have periodically plagued upland oak–hickory forests, particularly oak species in the red oak group, across the Ozark Highlands of Missouri, Arkansas and Oklahoma since the late 1970s. Advanced tree age and periodic drought, as well as Armillaria root fungi and oak borer attack are believed to contribute to oak decline and mortality....

Metabolic analysis of the synthesis of high levels of intracellular human SOD in Saccharomyces cerevisiae rhSOD 2060 411 SGA122.

PubMed

Gonzalez, Ramon; Andrews, Barbara A; Molitor, Julia; Asenjo, Juan A

2003-04-20

The synthesis of human superoxide dismutase (SOD) in batch cultures of a Saccharomyces cerevisiae strain using a glucose-limited minimal medium was studied through metabolic flux analysis. A stoichiometric model was built, which included 78 reactions, according to metabolic pathways operative in these strains during respirofermentative and oxidative metabolism. It allowed calculation of the distribution of metabolic fluxes during diauxic growth on glucose and ethanol. Fermentation profiles and metabolic fluxes were analyzed at different phases of diauxic growth for the recombinant strain (P+) and for its wild type (P-). The synthesis of SOD by the strain P+ resulted in a decrease in specific growth rate of 34 and 54% (growth on glucose and ethanol respectively) in comparison to the wild type. Both strains exhibited similar flux of glucose consumption and ethanol synthesis but important differences in carbon distribution with biomass/substrate yields and ATP production 50% higher in P-. A higher contribution of fermentative metabolism, with 64% of the energy produced at the phosphorylation level, was observed during SOD production. The flux of precursors to amino acids and nucleotides was higher in the recombinant strain, in agreement with the higher total RNA and protein levels. Lower specific growth rates in strain P+ appear to be related to the decrease in the rate of synthesis of nonrecombinant protein, as well as a decrease in the activities of the pentose phosphate (PP) pathway and TCA cycle. A very different way of entry into the stationary phase was observed for each strain: in the wild-type strain most metabolic fluxes decreased and fluxes related to energy reserve synthesis increased, while in the P+ strain the flux of 22 reactions (including PP pathway and amino acids biosynthesis) related to SOD production increased their fluxes. Changes in SOD production rates at different physiological states appear to be related to the differences in building blocks

Axonal Mitochondrial Clusters Containing Mutant SOD1 in Transgenic Models of ALS

PubMed Central

Lepanto, Paola; Elizondo, Victoria; Horjales, Sofia; Palacios, Florencia; Martinez-Palma, Laura; Marin, Monica; Beckman, Joseph S.

2009-01-01

Abstract We studied the subcellular distribution of mitochondria and superoxide dismutase-1 (SOD1) in whole mounts of microdissected motor axons of rats expressing the ALS-linked SOD1-G93A mutation. The rationale was to determine whether physical interactions between the enzyme and mitochondria were linked to the axonopathy of motor fibers occurring in amyotrophic lateral sclerosis (ALS). Mitochondria and SOD1 displayed a homogeneous distribution along motor axons both in nontransgenic rats and in those overexpressing wild-type SOD1. In contrast, axons from SOD1-G93A rats (older than 35 days) showed accumulation of mitochondria in discrete clusters located at regular intervals. Most of SOD1 immunoreactivity was enriched in these clusters and colocalized with mitochondria, suggesting a recruitment of SOD1-G93A to the organelle. The SOD1/mitochondrial clusters were abundant in motor axons but scarcely seen in sensory axons. Clusters also were stained for neuronal nitric oxide synthase, nitrotyrosine, and cytochrome c. The later also was detected surrounding clusters. Ubiquitin colocalized with clusters only at late stages of the disease. The cytoskeleton was not overtly altered in clusters. These results suggest that mutant SOD1 and defective mitochondria create localized dysfunctional domains in motor axons, which may lead to progressive axonopathy in ALS. Antioxid. Redox Signal. 11, 1535–1545. PMID:19344250

The activity of superoxide dismutases (SODs) at the early stages of wheat deetiolation

PubMed Central

Zimak-Piekarczyk, Paulina; Ślesak, Ireneusz

2018-01-01

Unbound tetrapyrroles, i.e. protochlorophyllide (Pchlide), chlorophyllide and chlorophylls, bring the risk of reactive oxygen species (ROS) being generated in the initial stages of angiosperm deetiolation due to inefficient usage of the excitation energy for photosynthetic photochemistry. We analyzed the activity of superoxide dismutases (SODs) in etiolated wheat (Triticum aestivum) leaves and at the beginning of their deetiolation. Mn-SOD and three isoforms of Cu/Zn-SODs were identified both in etiolated and greening leaves of T. aestivum. Two Cu/Zn-SODs, denoted as II and III, were found in plastids. The activity of plastidic Cu/Zn-SOD isoforms as well as that of Mn-SOD correlated with cell aging along a monocot leaf, being the highest at leaf tips. Moreover, a high Pchlide content at leaf tips was observed. No correlation between SOD activity and the accumulation of photoactive Pchlide, i.e. Pchlide bound into ternary Pchlide:Pchlide oxidoreductase:NADPH complexes was found. Cu/Zn-SOD I showed the highest activity at the leaf base. A flash of light induced photoreduction of the photoactive Pchlide to chlorophyllide as well as an increase in all the SODs activity which occurred in a minute time-scale. In the case of seedlings that were deetiolated under continuous light of moderate intensity (100 μmol photons m-2 s-1), only some fluctuations in plastidic Cu/Zn-SODs and Mn-SOD within the first four hours of greening were noticed. The activity of SODs is discussed with respect to the assembly of tetrapyrroles within pigment-protein complexes, monitored by fluorescence spectroscopy at 77 K. PMID:29558520

ATM is required for SOD2 expression and homeostasis within the mammary gland.

PubMed

Dyer, Lisa M; Kepple, Jessica D; Ai, Lingbao; Kim, Wan-Ju; Stanton, Virginia L; Reinhard, Mary K; Backman, Lindsey R F; Streitfeld, W Scott; Babu, Nivetha Ramesh; Treiber, Nicolai; Scharffetter-Kochanek, Karin; McKinnon, Peter J; Brown, Kevin D

2017-12-01

ATM activates the NF-κB transcriptional complex in response to genotoxic and oxidative stress. The purpose of this study was to examine if the NF-κB target gene and critical antioxidant SOD2 (MnSOD) in cultured mammary epithelium is also ATM-dependent, and what phenotypes arise from deletion of ATM and SOD2 within the mammary gland. SOD2 expression was studied in human mammary epithelial cells and MCF10A using RNAi to knockdown ATM or the NF-κB subunit RelA. To study ATM and SOD2 function in mammary glands, mouse lines containing Atm or Sod2 genes containing LoxP sites were mated with mice harboring Cre recombinase under the control of the whey acidic protein promoter. Quantitative PCR was used to measure gene expression, and mammary gland structure was studied using histology. SOD2 expression is ATM- and RelA-dependent, ATM knockdown renders cells sensitive to pro-oxidant exposure, and SOD mimetics partially rescue this sensitivity. Mice with germline deletion of Atm fail to develop mature mammary glands, but using a conditional knockout approach, we determined that Atm deletion significantly diminished the expression of Sod2. We also observed that these mice (termed Atm Δ/Δ ) displayed a progressive lactation defect as judged by reduced pup growth rate, aberrant lobulo-alveolar structure, diminished milk protein gene expression, and increased apoptosis within lactating glands. This phenotype appears to be linked to dysregulated Sod2 expression as mammary gland-specific deletion of Sod2 phenocopies defects observed in Atm Δ/Δ dams. We conclude that ATM is required to promote expression of SOD2 within the mammary epithelium, and that both ATM and SOD2 play a crucial role in mammary gland homeostasis.

Nitric oxide activates superoxide dismutase and ascorbate peroxidase to repress the cell death induced by wounding.

PubMed

Lin, Chih-Ching; Jih, Pei-Ju; Lin, Hsin-Hung; Lin, Jeng-Shane; Chang, Ling-Lan; Shen, Yu-Hsing; Jeng, Shih-Tong

2011-10-01

Wounding caused by rain, wind, and pathogen may lead plants to onset defense response. Previous studies indicated that mechanical wounding stimulates plants to generate nitric oxide (NO) and hydrogen peroxide (H(2)O(2)). In this study, the functions of NO and H(2)O(2) after wounding in sweet potato (Ipomoea batatas cv. Tainung 57) was further analyzed. Mechanical wounding damaged cells and resulted in necrosis, but the presence of NO donors or NO scavenger might reduce or enhance the cell death caused by wounding, respectively. The amount of H(2)O(2) induced by wounding was also decreased or increased when plants were incubated with NO donors or NO scavenger, individually. These results indicate that NO may regulate H(2)O(2) generation to affect cell death. NO-induced proteins isolated from two-dimensional electrophoresis were identified to be Copper/Zinc superoxide dismutases (CuZnSODs). The activities of CuZnSODs and ascorbate peroxidase (APX) could be enhanced by NO. In addition, the expression of CuZnSOD and APX was induced by wounding via NO, and their expression was further stimulated by NO through the generation of cGMP. The influx of calcium ions and the activity of NADPH oxidase were also involved in the NO signal transduction pathway inducing APX expression. Collectively, the generation of H(2)O(2) in wounded plants might trigger cell death. Meanwhile, the production of NO induced by wounding stimulated signal transducers including cGMP, calcium ions, and H(2)O(2) to activate CuZnSOD and APX, which further decreased H(2)O(2) level and reduced the cell death caused by wounding.

Sulfuryl fluoride fumigation of red oak logs eradicates the oak wilt fungus

Treesearch

Elmer L. Schmidt; Jennifer Juzwik; Brian Schneider

1997-01-01

Preliminary field trials using red oak logs from trees dying from oak wilt disease were successful in eliminating oak wilt fungus from sapwood after fumigation with sulfuryl fluoride for 72 h under tarp. These results support earlier laboratory data on the fungitoxicity of sulfuryl fluoride as a potential replacement for methyl bromide of exported red oak veneer logs....

AMELIORATION OF ETHANOL-INDUCED DYSMORPHOGENESIS BY ADENOVIRAL-MEDIATED CU,ZN-SOD AND MN-SOD EXPRESSION IN NEURULATION STAGED MOUSE EMBRYOS IN VITRO

EPA Science Inventory

AMELIORATION OF ETHANOL-INDUCED DYSMORPHOGENESIS BY ADENOVIRAL-MEDIATED Cu,Zn-SOD AND Mn-SOD EXPRESSION IN NEURULATION STAGED MOUSE EMBRYOS IN VITRO. JB Smith1, PC Hartig3, MR Blanton3, KK Sulik1,2, and ES Hunter3. 1Department of Cell and Developmental Biology and 2Bowles Cente...

Imaging of glial cell morphology, SOD1 distribution and elemental composition in the brainstem and hippocampus of the ALS hSOD1G93A rat.

PubMed

Stamenković, Stefan; Dučić, Tanja; Stamenković, Vera; Kranz, Alexander; Andjus, Pavle R

2017-08-15

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder affecting motor and cognitive domains of the CNS. Mutations in the Cu,Zn-superoxide dismutase (SOD1) cause 20% of familial ALS and provoke formation of intracellular aggregates and copper and zinc unbinding, leading to glial activation and neurodegeneration. Therefore, we investigated glial cell morphology, intracellular SOD1 distribution, and elemental composition in the brainstem and hippocampus of the hSOD1 G93A transgenic rat model of ALS. Immunostaining for astrocytes, microglia and SOD1 revealed glial proliferation and progressive tissue accumulation of SOD1 in both brain regions of ALS rats starting already at the presymptomatic stage. Glial cell morphology analysis in the brainstem of ALS rats revealed astrocyte activation occurring before disease symptoms onset, followed by activation of microglia. Hippocampal ALS astrocytes exhibited an identical reactive profile, while microglial morphology was unchanged. Additionally, ALS brainstem astrocytes demonstrated progressive SOD1 accumulation in the cell body and processes, while microglial SOD1 levels were reduced and its distribution limited to distal cell processes. In the hippocampus both glial cell types exhibited SOD1 accumulation in the cell body. X-ray fluorescence imaging revealed decreased P and increased Ca, Cl, K, Ni, Cu and Zn in the brainstem, and higher levels of Cl, Ni and Cu, but lower levels of Zn in the hippocampus of symptomatic ALS rats. These results bring new insights into the glial response during disease development and progression in motor as well as in non-motor CNS structures, and indicate disturbed tissue elemental homeostasis as a prominent hallmark of disease pathology. Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.

Exposure of Bacterial Biofilms to Electrical Current Leads to Cell Death Mediated in Part by Reactive Oxygen Species

PubMed Central

Brinkman, Cassandra L.; Schmidt-Malan, Suzannah M.; Karau, Melissa J.; Greenwood-Quaintance, Kerryl; Hassett, Daniel J.; Mandrekar, Jayawant N.

2016-01-01

Bacterial biofilms may form on indwelling medical devices such as prosthetic joints, heart valves and catheters, causing challenging-to-treat infections. We have previously described the ‘electricidal effect’, in which bacterial biofilms are decreased following exposure to direct electrical current. Herein, we sought to determine if the decreased bacterial quantities are due to detachment of biofilms or cell death and to investigate the role that reactive oxygen species (ROS) play in the observed effect. Using confocal and electron microscopy and flow cytometry, we found that direct current (DC) leads to cell death and changes in the architecture of biofilms formed by Gram-positive and Gram-negative bacteria. Reactive oxygen species (ROS) appear to play a role in DC-associated cell death, as there was an increase in ROS-production by Staphylococcus aureus and Staphylococcus epidermidis biofilms following exposure to DC. An increase in the production of ROS response enzymes catalase and superoxide dismutase (SOD) was observed for S. aureus, S. epidermidis and Pseudomonas aeruginosa biofilms following exposure to DC. Additionally, biofilms were protected from cell death when supplemented with antioxidants and oxidant scavengers, including catalase, mannitol and Tempol. Knocking out SOD (sodAB) in P. aeruginosa led to an enhanced DC effect. Microarray analysis of P. aeruginosa PAO1 showed transcriptional changes in genes related to the stress response and cell death. In conclusion, the electricidal effect results in death of bacteria in biofilms, mediated, at least in part, by production of ROS. PMID:27992529

Exposure of Bacterial Biofilms to Electrical Current Leads to Cell Death Mediated in Part by Reactive Oxygen Species.

PubMed

Brinkman, Cassandra L; Schmidt-Malan, Suzannah M; Karau, Melissa J; Greenwood-Quaintance, Kerryl; Hassett, Daniel J; Mandrekar, Jayawant N; Patel, Robin

2016-01-01

Bacterial biofilms may form on indwelling medical devices such as prosthetic joints, heart valves and catheters, causing challenging-to-treat infections. We have previously described the 'electricidal effect', in which bacterial biofilms are decreased following exposure to direct electrical current. Herein, we sought to determine if the decreased bacterial quantities are due to detachment of biofilms or cell death and to investigate the role that reactive oxygen species (ROS) play in the observed effect. Using confocal and electron microscopy and flow cytometry, we found that direct current (DC) leads to cell death and changes in the architecture of biofilms formed by Gram-positive and Gram-negative bacteria. Reactive oxygen species (ROS) appear to play a role in DC-associated cell death, as there was an increase in ROS-production by Staphylococcus aureus and Staphylococcus epidermidis biofilms following exposure to DC. An increase in the production of ROS response enzymes catalase and superoxide dismutase (SOD) was observed for S. aureus, S. epidermidis and Pseudomonas aeruginosa biofilms following exposure to DC. Additionally, biofilms were protected from cell death when supplemented with antioxidants and oxidant scavengers, including catalase, mannitol and Tempol. Knocking out SOD (sodAB) in P. aeruginosa led to an enhanced DC effect. Microarray analysis of P. aeruginosa PAO1 showed transcriptional changes in genes related to the stress response and cell death. In conclusion, the electricidal effect results in death of bacteria in biofilms, mediated, at least in part, by production of ROS.

Riluzole But Not Melatonin Ameliorates Acute Motor Neuron Degeneration and Moderately Inhibits SOD1-Mediated Excitotoxicity Induced Disrupted Mitochondrial Ca2+ Signaling in Amyotrophic Lateral Sclerosis

PubMed Central

Jaiswal, Manoj Kumar

2017-01-01

Selective motoneurons (MNs) degeneration in the brain stem, hypoglossal motoneurons (HMNs), and the spinal cord resulting in patients paralysis and eventual death are prominent features of amyotrophic lateral sclerosis (ALS). Previous studies have suggested that mitochondrial respiratory impairment, low Ca2+ buffering and homeostasis and excitotoxicity are the pathological phenotypes found in mice, and cell culture models of familial ALS (fALS) linked with Cu/Zn-superoxide dismutase 1 (SOD1) mutation. In our study, we aimed to understand the impact of riluzole and melatonin on excitotoxicity, neuronal protection and Ca2+ signaling in individual HMNs ex vivo in symptomatic adult ALS mouse brain stem slice preparations and in WT and SOD1-G93A transfected SH-SY5Y neuroblastoma cell line using fluorescence microscopy, calcium imaging with high speed charged coupled device camera, together with immunohistochemistry, cell survival assay and histology. In our experiments, riluzole but not melatonin ameliorates MNs degeneration and moderately inhibit excitotoxicity and cell death in SH-SY5YWT or SH-SY5YG93A cell lines induced by complex IV blocker sodium azide. In brain stem slice preparations, riluzole significantly inhibit HMNs cell death induced by inhibiting the mitochondrial electron transport chain by Na-azide. In the HMNs of brainstem slice prepared from adult (14–15 weeks) WT, and corresponding symptomatic SOD1G93A mice, we measured the effect of riluzole and melatonin on [Ca2+]i using fura-2 AM ratiometric calcium imaging in individual MNs. Riluzole caused a significant decrease in [Ca2+]i transients and reversibly inhibited [Ca2+]i transients in Fura-2 AM loaded HMNs exposed to Na-azide in adult symptomatic SOD1G93A mice. On the contrary, melatonin failed to show similar effects in the HMNs of WT and SOD1G93A mice. Intrinsic nicotinamide adenine dinucleotide (NADH) fluorescence, an indicator of mitochondrial metabolism and health in MNs, showed enhanced

A Phase I, Randomised, First-in-Human Study of an Antisense Oligonucleotide Directed Against SOD1 Delivered Intrathecally in SOD1-Familial ALS Patients

PubMed Central

Miller, Timothy; Pestronk, Alan; David, William; Rothstein, Jeffrey; Simpson, Ericka; Appel, Stanley H.; Andres, Patricia L.; Mahoney, Katy; Allred, Peggy; Alexander, Katie; Ostrow, Lyle W.; Schoenfeld, David; Macklin, Eric A.; Norris, Daniel A.; Manousakis, Georgios; Crisp, Matthew; Smith, Richard; Bennett, C.F.; Bishop, Kathie; Cudkowicz, Merit E

2013-01-01

Objective To evaluate the safety, tolerability, and pharmacokinetics of an antisense oligonucleotide designed to inhibit SOD1 expression (ISIS 333611) following intrathecal administration in patients with SOD1-related familial amyotrophic lateral sclerosis (ALS). Background Mutations in SOD1 cause 13% of familial ALS. In animal studies, ISIS 333611 delivered to the cerebrospinal fluid (CSF) distributed to the brain and spinal cord, decreased SOD1 mRNA and protein levels in spinal cord tissue, and prolonged survival in the SOD1G93A rat ALS model. Methods In a randomized, placebo controlled Phase 1 trial, ISIS 333611 was delivered by intrathecal infusion using an external pump over 11.5 hours at increasing doses to four cohorts of eight SOD1 positive ALS subjects (randomized 6 drug: 2 placebo/cohort). Subjects were allowed to re-enroll in subsequent cohorts. Safety and tolerability assessments were made during the infusion and periodically over 28 days following the infusion. CSF and plasma drug levels were measured. Findings No dose-limiting toxicities were identified at doses up to 3.0 mg. No safety or tolerability concerns related to ISIS 333611 were identified. There were no serious adverse events (AEs) in ISIS 333611-treated subjects. Re-enrollment and re-dosing of subjects with ISIS 333611 was also well tolerated. Dose-dependent CSF and plasma concentrations were observed. Interpretation In this first clinical study to report intrathecal delivery of an antisense oligonucleotide, ISIS 333611 was well tolerated when administered as an intrathecal infusion in subjects with SOD1 familial ALS. CSF and plasma drug levels were consistent with levels predicted from preclinical studies. These results suggest that antisense oligonucleotide delivery to the central nervous system may be a feasible therapeutic strategy for neurological disorders. Source of funding ALS Association, Muscular Dystrophy Association, Isis Pharmaceuticals PMID:23541756

A Comparison of Two Yeast MnSODs: Mitochondrial Saccharomyces cerevisiae versus Cytosolic Candida albicans

DOE Office of Scientific and Technical Information (OSTI.GOV)

Sheng Y.; Cabelli D.; Stich, T.A.

Human MnSOD is significantly more product-inhibited than bacterial MnSODs at high concentrations of superoxide (O{sub 2}{sup -}). This behavior limits the amount of H{sub 2}O{sub 2} produced at high [O{sub 2}{sup -}]; its desirability can be explained by the multiple roles of H{sub 2}O{sub 2} in mammalian cells, particularly its role in signaling. To investigate the mechanism of product inhibition in MnSOD, two yeast MnSODs, one from Saccharomyces cerevisiae mitochondria (ScMnSOD) and the other from Candida albicans cytosol (CaMnSODc), were isolated and characterized. ScMnSOD and CaMnSODc are similar in catalytic kinetics, spectroscopy, and redox chemistry, and they both rest predominantlymore » in the reduced state (unlike most other MnSODs). At high [O{sub 2}{sup -}], the dismutation efficiencies of the yeast MnSODs surpass those of human and bacterial MnSODs, due to very low level of product inhibition. Optical and parallel-mode electron paramagnetic resonance (EPR) spectra suggest the presence of two Mn{sup 3+} species in yeast Mn{sup 3+}SODs, including the well-characterized 5-coordinate Mn{sup 3+} species and a 6-coordinate L-Mn{sup 3+} species with hydroxide as the putative sixth ligand (L). The first and second coordination spheres of ScMnSOD are more similar to bacterial than to human MnSOD. Gln154, an H-bond donor to the Mn-coordinated solvent molecule, is slightly further away from Mn in yeast MnSODs, which may result in their unusual resting state. Mechanistically, the high efficiency of yeast MnSODs could be ascribed to putative translocation of an outer-sphere solvent molecule, which could destabilize the inhibited complex and enhance proton transfer from protein to peroxide. Our studies on yeast MnSODs indicate the unique nature of human MnSOD in that it predominantly undergoes the inhibited pathway at high [O{sub 2}{sup -}].« less

A Comparison of Two Yeast MnSODs: Mitochondrial Saccharomyces cerevisiae versus Cytosolic Candida albicans

PubMed Central

Sheng, Yuewei; Stich, Troy A.; Barnese, Kevin; Gralla, Edith B.; Cascio, Duilio; Britt, R. David; Cabelli, Diane E.; Valentine, Joan Selverstone

2011-01-01

Human MnSOD is significantly more product-inhibited than bacterial MnSODs at high concentrations of superoxide (O2−). This behavior limits the amount of H2O2 produced at high [O2−]; its desirability can be explained by the multiple roles of H2O2 in mammalian cells, particularly its role in signaling. To investigate the mechanism of product inhibition in MnSOD, two yeast MnSODs, one from Saccharomyces cerevisiae mitochondria (ScMnSOD) and the other from Candida albicans cytosol (CaMnSODc), were isolated and characterized. ScMnSOD and CaMnSODc are similar in catalytic kinetics, spectroscopy and redox chemistry, and they both rest predominantly in the reduced state (unlike most other MnSODs). At high [O2−] the dismutation efficiencies of the yeast MnSODs surpass those of human and bacterial MnSODs, due to very low level of product inhibition. Optical and parallel-mode electron paramagnetic resonance (EPR) spectra suggest the presence of two Mn3+ species in yeast Mn3+SODs, including the well-characterized 5-coordinate Mn3+ species and a 6-coordinate L-Mn3+ species with hydroxide as the putative sixth ligand (L). The first and second coordination spheres of ScMnSOD are more similar to bacterial than to human MnSOD. Gln154, an H-bond donor to the Mn-coordinated solvent molecule, is slightly further away from Mn in yeast MnSODs, which may result in their unusual resting state. Mechanistically, the high efficiency of yeast MnSODs could be ascribed to putative translocation of an outer-sphere solvent molecule, which could destabilize the inhibited complex and enhance proton transfer from protein to peroxide. Our studies on yeast MnSODs indicate the unique nature of human MnSOD in that it predominantly undergoes the inhibited pathway at high [O2−]. PMID:22077216

Insect damage to oaks

Treesearch

Charles O. Rexrode

1971-01-01

In terms of mortality caused by insects, defoliators are the most serious enemies of oaks at the present time. An oak leaf tier, Croesia semipurprana, is one of the principal defoliators of trees in the red oak group. Oak leaf rollers, primarily Archips semiferana, have been responsible for widespread mortality in white and...

Androgens affect muscle, motor neuron, and survival in a mouse model of SOD1-related amyotrophic lateral sclerosis.

PubMed

Aggarwal, Tanya; Polanco, Maria J; Scaramuzzino, Chiara; Rocchi, Anna; Milioto, Carmelo; Emionite, Laura; Ognio, Emanuela; Sambataro, Fabio; Galbiati, Mariarita; Poletti, Angelo; Pennuto, Maria

2014-08-01

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by selective loss of upper and lower motor neurons and skeletal muscle atrophy. Epidemiologic and experimental evidence suggest the involvement of androgens in ALS pathogenesis, but the mechanism through which androgens modify the ALS phenotype is unknown. Here, we show that androgen ablation by surgical castration extends survival and disease duration of a transgenic mouse model of ALS expressing mutant human SOD1 (hSOD1-G93A). Furthermore, long-term treatment of orchiectomized hSOD1-G93A mice with nandrolone decanoate (ND), an anabolic androgenic steroid, worsened disease manifestations. ND treatment induced muscle fiber hypertrophy but caused motor neuron death. ND negatively affected survival, thereby dissociating skeletal muscle pathology from life span in this ALS mouse model. Interestingly, orchiectomy decreased androgen receptor levels in the spinal cord and muscle, whereas ND treatment had the opposite effect. Notably, stimulation with ND promoted the recruitment of endogenous androgen receptor into biochemical complexes that were insoluble in sodium dodecyl sulfate, a finding consistent with protein aggregation. Overall, our results shed light on the role of androgens as modifiers of ALS pathogenesis via dysregulation of androgen receptor homeostasis. Copyright © 2014 Elsevier Inc. All rights reserved.

Response of white oak and black oak seedlings to a mid-story removal

Treesearch

Dylan N. Dillaway; Jeff Stringer

2005-01-01

White oak (Quercus alba L.) and black oak (Quercus velutina Lam.) often dominate stands on intermediate to high quality sites. In these stands there is often a bank of advanced oak regeneration (>1 ft. tall) in place. However, this advanced oak regeneration rarely achieves a co-dominant or dominant status when a regeneration...

Host-induced genome alterations in Phytophthora ramorum, I. NA1 lineage on coast live oak in California, II. EU1 lineage on Chamaecyparis lawsoniana in UK

Treesearch

Takao Kasuga; Mai Bui; Elizabeth Bernhardt; Tedmund Swiecki; Kamyar Aram; Lien Bertier; Jennifer Yuzon; Liliana M. Cano; Joan Webber; Clive Brasier; Caroline Press; Niklaus Grünwald; David Rizzo; Matteo Garbelotto

2017-01-01

Rapid phenotypic diversification in clonal invasive populations is often observed, although the underlying genetic mechanisms remain elusive. Lineages of the sudden oak death pathogen Phytophthora ramorum are exclusively clonal, yet isolates of the NA1 lineage from oak (Quercus spp.) frequently exhibit...

MnSOD expression inhibited by electromagnetic pulse radiation in the rat testis.

PubMed

Zeng, LiHua; Ji, XiTuan; Zhang, YanJun; Miao, Xia; Zou, ChangXu; Lang, HaiYang; Zhang, Jie; Li, YuRong; Wang, XiaoWu; Qi, HongXing; Ren, DongQin; Guo, GuoZhen

2011-12-01

Male Sprague Dawley rats were exposed to EMP irradiation of 100 kV/m peak-to-peak e-field intensity and different numbers of pulses. Rat sperm samples were prepared for analysis of sperm qualities; Testes were assessed by transmission electron microscopy and serum hormone concentrations were examined by radioimmunoassay; Enzymatic activities of Total-superoxide dismutase(T-SOD) and manganese-superoxide dismutase (MnSOD), the mRNA levels of MnSOD and cuprozinc-superoxide dismutase (CuZnSOD), and the density of malondialdehyde (MDA) were also determined. EMP irradiation did not affect spermatozoon morphology, micronucleus formation rate, sperm number or viability, but the acrosin reaction rate decreased at 24 h and 48 h and recovered by 72 h after irradiation as compared to the controls. The ultrastructure of rat testis displayed more serious damage at 24 h than at other time points (6 h, 12 h, 48 h). Serum levels of luteotrophic hormone (LH) and testosterone (T) were elevated in irradiated rats as compared to controls. After irradiation, enzymatic activities of T-SOD and MnSOD were reduced by 24 h, consistent with the changes observed in MnSOD mRNA expression; MDA content increased at 6 h in turn. These studies have quantified the morphological damage and dysfunction in the rat reproductive system induced by EMP. The mechanism of EMP induced damage may be associated with the inhibition of MnSOD expression.

People and oaks

Treesearch

Paul F. Starrs

2015-01-01

While technical knowledge of oaks, acorns, habitat, wildlife, and woodland environments is evolving and a sought-after field of study, there are profound linkages, at once humanistic and artistic, where it comes to people and oaks. Looking at six distinct facets of humans and oak woodlands, this essay suggests that the bonds of people to place can be mediated by the...

Great oaks from little acorns grow: planting native oak in the Pacific Northwest

Treesearch

Gail Wells; Warren Devine; Connie Harrington

2010-01-01

The decline of oak woodlands is an urgent conservation challenge in the Pacific Northwest. Prior to settlement by Euro-Americans, prairies, oak-dominated savannas, and oak woodlands were abundant in the low-lying areas of the region. Now it’s estimated that 1 to 5 percent of that native oak savanna remains. The rest has been supplanted by pastures, fields, Douglas-fir...

Manganese superoxide dismutase, MnSOD and its mimics.

PubMed

Miriyala, Sumitra; Spasojevic, Ivan; Tovmasyan, Artak; Salvemini, Daniela; Vujaskovic, Zeljko; St Clair, Daret; Batinic-Haberle, Ines

2012-05-01

Increased understanding of the role of mitochondria under physiological and pathological conditions parallels increased exploration of synthetic and natural compounds able to mimic MnSOD - endogenous mitochondrial antioxidant defense essential for the existence of virtually all aerobic organisms from bacteria to humans. This review describes most successful mitochondrially-targeted redox-active compounds, Mn porphyrins and MitoQ(10) in detail, and briefly addresses several other compounds that are either catalysts of O(2)(-) dismutation, or its non-catalytic scavengers, and that reportedly attenuate mitochondrial dysfunction. While not a true catalyst (SOD mimic) of O(2)(-) dismutation, MitoQ(10) oxidizes O(2)(-) to O(2) with a high rate constant. In vivo it is readily reduced to quinol, MitoQH(2), which in turn reduces ONOO(-) to NO(2), producing semiquinone radical that subsequently dismutes to MitoQ(10) and MitoQH(2), completing the "catalytic" cycle. In MitoQ(10), the redox-active unit was coupled via 10-carbon atom alkyl chain to monocationic triphenylphosphonium ion in order to reach the mitochondria. Mn porphyrin-based SOD mimics, however, were designed so that their multiple cationic charge and alkyl chains determine both their remarkable SOD potency and carry them into the mitochondria. Several animal efficacy studies such as skin carcinogenesis and UVB-mediated mtDNA damage, and subcellular distribution studies of Saccharomyces cerevisiae and mouse heart provided unambiguous evidence that Mn porphyrins mimic the site and action of MnSOD, which in turn contributes to their efficacy in numerous in vitro and in vivo models of oxidative stress. Within a class of Mn porphyrins, lipophilic analogs are particularly effective for treating central nervous system injuries where mitochondria play key role. This article is part of a Special Issue entitled: Antioxidants and Antioxidant Treatment in Disease. Copyright © 2011 Elsevier B.V. All rights reserved.

Red Oak Borer

Treesearch

D. E. Donley; R.E. Acciavatti

1980-01-01

The red oak borer, Enaphalodes rufulus (Haldeman)3, is an important member of the oak borer complex that permanently damages the wood of living oak trees and causes a decrease in lumber grade. The loss in grade can amount to 40 percent of the current tree value, which, at today's prices, is about $80 per thousand board feet for factory grade lumber in terms of...

Isolated cytochrome c oxidase deficiency in G93A SOD1 mice overexpressing CCS protein.

PubMed

Son, Marjatta; Leary, Scot C; Romain, Nadine; Pierrel, Fabien; Winge, Dennis R; Haller, Ronald G; Elliott, Jeffrey L

2008-05-02

G93A SOD1 transgenic mice overexpressing CCS protein develop an accelerated disease course that is associated with enhanced mitochondrial pathology and increased mitochondrial localization of mutant SOD1. Because these results suggest an effect of mutant SOD1 on mitochondrial function, we assessed the enzymatic activities of mitochondrial respiratory chain complexes in the spinal cords of CCS/G93A SOD1 and control mice. CCS/G93A SOD1 mouse spinal cord demonstrates a 55% loss of complex IV (cytochrome c oxidase) activity compared with spinal cord from age-matched non-transgenic or G93A SOD1 mice. In contrast, CCS/G93A SOD1 spinal cord shows no reduction in the activities of complex I, II, or III. Blue native gel analysis further demonstrates a marked reduction in the levels of complex IV but not of complex I, II, III, or V in spinal cords of CCS/G93A SOD1 mice compared with non-transgenic, G93A SOD1, or CCS/WT SOD1 controls. With SDS-PAGE analysis, spinal cords from CCS/G93A SOD1 mice showed significant decreases in the levels of two structural subunits of cytochrome c oxidase, COX1 and COX5b, relative to controls. In contrast, CCS/G93A SOD1 mouse spinal cord showed no reduction in levels of selected subunits from complexes I, II, III, or V. Heme A analyses of spinal cord further support the existence of cytochrome c oxidase deficiency in CCS/G93A SOD1 mice. Collectively, these results establish that CCS/G93A SOD1 mice manifest an isolated complex IV deficiency which may underlie a substantial part of mutant SOD1-induced mitochondrial cytopathy.

Knocking down metabotropic glutamate receptor 1 improves survival and disease progression in the SOD1(G93A) mouse model of amyotrophic lateral sclerosis.

PubMed

Milanese, Marco; Giribaldi, Francesco; Melone, Marcello; Bonifacino, Tiziana; Musante, Ilaria; Carminati, Enrico; Rossi, Pia I A; Vergani, Laura; Voci, Adriana; Conti, Fiorenzo; Puliti, Aldamaria; Bonanno, Giambattista

2014-04-01

Amyotrophic lateral sclerosis (ALS) is a late-onset fatal neurodegenerative disease reflecting degeneration of upper and lower motoneurons (MNs). The cause of ALS and the mechanisms of neuronal death are still largely obscure, thus impairing the establishment of efficacious therapies. Glutamate (Glu)-mediated excitotoxicity plays a major role in MN degeneration in ALS. We recently demonstrated that the activation of Group I metabotropic Glu autoreceptors, belonging to both type 1 and type 5 receptors (mGluR1 and mGluR5), at glutamatergic spinal cord nerve terminals, produces excessive Glu release in mice over-expressing human superoxide-dismutase carrying the G93A point mutation (SOD1(G93A)), a widely used animal model of human ALS. To establish whether these receptors are implicated in ALS, we generated mice expressing half dosage of mGluR1 in the SOD1(G93A) background (SOD1(G93A)Grm1(crv4/+)), by crossing the SOD1(G93A) mutant mouse with the Grm1(crv4/+) mouse, lacking mGluR1 because of a spontaneous recessive mutation. SOD1(G93A)Grm1(crv4/+) mice showed prolonged survival probability, delayed pathology onset, slower disease progression and improved motor performances compared to SOD1(G93A) mice. These effects were associated to reduction of mGluR5 expression, enhanced number of MNs, decreased astrocyte and microglia activation, normalization of metallothionein and catalase mRNA expression, reduced mitochondrial damage, and decrease of abnormal Glu release in spinal cord of SOD1(G93A)Grm1(crv4/+)compared to SOD1(G93A) mice. These results demonstrate that a lower constitutive level of mGluR1 has a significant positive impact on mice with experimental ALS, thus providing the rationale for future pharmacological approaches to ALS by selectively blocking Group I metabotropic Glu receptors. Copyright © 2013 The Authors. Published by Elsevier Inc. All rights reserved.

DOLLY SODS WILDERNESS, WEST VIRGINIA.

USGS Publications Warehouse

Englund, Kenneth J.; Hill, James J.

1984-01-01

Coal, the principal mineral resource of the Dolly Sods Wilderness, West Virginia is in at least seven beds of low- to medium-volatile bituminous rank. Of these beds, four are of sufficient thickness, quality, and extent to contain demonstrated coal resources which are estimated to total about 15. 5 million short tons in areas of substantiated coal resource potential. A Small-scale development of the coal resources of the Dolly Sods Wilderness has been by several shallow adits which provided fuel for locomotives during early logging operations and by a one truck mine. All mine entries are now abandoned. Peat, shale, clay, and sandstone, occur in the area but because of remoteness of markets and inaccessability they are not classified as resources in this report. Natural gas may occur in rocks underlying the area, but because of a lack of subsurface information an estimate of resource potential has not been made. No evidence of metallic-mineral resources was found during this investigation.

Risk analysis and guidelines for harvest activities in wisconsin oak timberlands to minimize oak wilt threat

Treesearch

Jennifer Juzwik; Jane Cummings-Carlson; Kyoko Scanlon

2010-01-01

Oaks (Quercus spp.) are an important species group in the forests of Wisconsin. The State’s timberland typed as oak-hickory forest was estimated at 2.9 million acres in 1996. Growing stock volume for red oak was estimated at 2.4 billion cubic feet, whereas select white oak volume was estimated to be 927 million cubic feet. Oak wilt, the oak disease...

Effect of CCS on the Accumulation of FALS SOD1 Mutant-containing Aggregates and on Mitochondrial Translocation of SOD1 Mutants: Implication of a Free Radical Hypothesis

PubMed Central

Kim, Ha Kun; Chung, Youn Wook; Chock, P. Boon; Yim, Moon B.

2011-01-01

Missense mutations of SOD1 are linked to familial amyotrophic lateral sclerosis (FALS) through a yet-to-be identified toxic-gain-of-function. One of the proposed mechanisms involves enhanced aggregate formation. However, a recent study showed that dual transgenic mice overexpressing both G93A and CCS copper chaperone (G93A/CCS) exhibit no SOD1-positive aggregates yet show accelerated FALS symptoms with enhanced mitochondrial pathology compared to G93A mice. Using a dicistronic mRNA to simultaneously generate hSOD1 mutants, G93A, A4V and G85R, and hCCS in AAV293 cells, we revealed: (i) CCS is degraded primarily via a macroautophagy pathway. It forms a stable heterodimer with inactive G85R, and via its novel copper chaperone-independent molecular chaperone activity facilitates G85R degradation via a macroautophagy-mediated pathway. For active G93A and A4V, CCS catalyzes their maturation to form active and soluble homodimers. (ii) CCS reduces, under non-oxidative conditions, yet facilitates in the presence of H2O2, mitochondrial translocation of inactive SOD1 mutants. These results, together with previous reports showing FALS SOD1 mutants enhanced free radical-generating activity, provide a mechanistic explanation for the observations with G93A/CCS dual transgenic mice and suggest that free radical generation by FALS SOD1, enhanced by CCS, may, in part, be responsible for the FALS SOD1 mutant-linked aggregation, mitochondrial translocation, and degradation. PMID:21354101

Effect of CCS on the accumulation of FALS SOD1 mutant-containing aggregates and on mitochondrial translocation of SOD1 mutants: implication of a free radical hypothesis.

PubMed

Kim, Ha Kun; Chung, Youn Wook; Chock, P Boon; Yim, Moon B

2011-05-15

Missense mutations of SOD1 are linked to familial amyotrophic lateral sclerosis (FALS) through a yet-to-be identified toxic-gain-of-function. One of the proposed mechanisms involves enhanced aggregate formation. However, a recent study showed that dual transgenic mice overexpressing both G93A and CCS copper chaperone (G93A/CCS) exhibit no SOD1-positive aggregates yet show accelerated FALS symptoms with enhanced mitochondrial pathology compared to G93A mice. Using a dicistronic mRNA to simultaneously generate hSOD1 mutants, G93A, A4V and G85R, and hCCS in AAV293 cells, we revealed: (i) CCS is degraded primarily via a macroautophagy pathway. It forms a stable heterodimer with inactive G85R, and via its novel copper chaperone-independent molecular chaperone activity facilitates G85R degradation via a macroautophagy-mediated pathway. For active G93A and A4V, CCS catalyzes their maturation to form active and soluble homodimers. (ii) CCS reduces, under non-oxidative conditions, yet facilitates in the presence of H(2)O(2), mitochondrial translocation of inactive SOD1 mutants. These results, together with previous reports showing FALS SOD1 mutants enhanced free radical-generating activity, provide a mechanistic explanation for the observations with G93A/CCS dual transgenic mice and suggest that free radical generation by FALS SOD1, enhanced by CCS, may, in part, be responsible for the FALS SOD1 mutant-linked aggregation, mitochondrial translocation, and degradation. Published by Elsevier Inc.

Silvical characteristics of the five upland oaks

Treesearch

Earl L. Core

1971-01-01

The five most important upland oaks of eastern North America are white oak (Quercus alba), chestnut oak (Q. prinus), northern red oak (Q. rubra), black oak (Q. velutina), and scarlet oak (Q. coccinea). Of these, white oak and northern red oak are most characteristic of...

7 CFR 1437.309 - Turfgrass sod.

Code of Federal Regulations, 2011 CFR

2011-01-01

... stratum of soil bound by mature grass and plant roots into a thick mat produced in commercial quantities for sale. (b) Specific species, types or varieties of grass intended for turfgrass sod will be...

7 CFR 1437.309 - Turfgrass sod.

Code of Federal Regulations, 2010 CFR

2010-01-01

... stratum of soil bound by mature grass and plant roots into a thick mat produced in commercial quantities for sale. (b) Specific species, types or varieties of grass intended for turfgrass sod will be...

Sod2 haploinsufficiency does not accelerate aging of telomere dysfunctional mice

PubMed Central

Guachalla, Luis Miguel; Ju, Zhenyu; Koziel, Rafal; von Figura, Guido; Song, Zhangfa; Fusser, Markus; Epe, Bernd; Jansen-Dűrr, Pidder; Rudolph, K. Lenhard

2009-01-01

Telomere shortening represents a causal factor of cellular senescence. At the same time, several lines of evidence indicate a pivotal role of oxidative DNA damage for the aging process in vivo. A causal connection between the two observations was suggested by experiments showing accelerated telomere shorting under conditions of oxidative stress in cultured cells, but has never been studied in vivo. We therefore have analysed whether an increase in mitochondrial derived oxidative stress in response to heterozygous deletion of superoxide dismutase (Sod2+/-) would exacerbate aging phenotypes in telomere dysfunctional (mTerc-/-) mice. Heterozygous deletion of Sod2 resulted in reduced SOD2 protein levels and increased oxidative stress in aging telomere dysfunctional mice, but this did not lead to an increase in basal levels of oxidative nuclear DNA damage, an accumulation of nuclear DNA breaks, or an increased rate of telomere shortening in the mice. Moreover, heterozygous deletion of Sod2 did not accelerate the depletion of stem cells and the impairment in organ maintenance in aging mTerc-/- mice. In agreement with these observations, Sod2 haploinsufficiency did not lead to a further reduction in lifespan of mTerc-/- mice. Together, these results indicate that a decrease in SOD2-dependent antioxidant defence does not exacerbate aging in the context of telomere dysfunction. PMID:20195488

Altered Phenotypes in Saccharomyces cerevisiae by Heterologous Expression of Basidiomycete Moniliophthora perniciosa SOD2 Gene.

PubMed

Melo, Sônia C; Santos, Regineide X; Melgaço, Ana C; Pereira, Alanna C F; Pungartnik, Cristina; Brendel, Martin

2015-06-01

Heterologous expression of a putative manganese superoxide dismutase gene (SOD2) of the basidiomycete Moniliophthora perniciosa complemented the phenotypes of a Saccharomyces cerevisiae sod2Δ mutant. Sequence analysis of the cloned M. perniciosa cDNA revealed an open reading frame (ORF) coding for a 176 amino acid polypeptide with the typical metal-binding motifs of a SOD2 gene, named MpSOD2. Phylogenetic comparison with known manganese superoxide dismutases (MnSODs) located the protein of M. perniciosa (MpSod2p) in a clade with the basidiomycete fungi Coprinopsis cinerea and Laccaria bicolor. Haploid wild-type yeast transformants containing a single copy of MpSOD2 showed increased resistance phenotypes against oxidative stress-inducing hydrogen peroxide and paraquat, but had unaltered phenotype against ultraviolet-C (UVC) radiation. The same transformants exhibited high sensitivity against treatment with the pro-mutagen diethylnitrosamine (DEN) that requires oxidation to become an active mutagen/carcinogen. Absence of MpSOD2 in the yeast sod2Δ mutant led to DEN hyper-resistance while introduction of a single copy of this gene restored the yeast wild-type phenotype. The haploid yeast wild-type transformant containing two SOD2 gene copies, one from M. perniciosa and one from its own, exhibited DEN super-sensitivity. This transformant also showed enhanced growth at 37 °C on the non-fermentable carbon source lactate, indicating functional expression of MpSod2p. The pro-mutagen dihydroethidium (DHE)-based fluorescence assay monitored basal level of yeast cell oxidative stress. Compared to the wild type, the yeast sod2Δ mutant had a much higher level of intrinsic oxidative stress, which was reduced to wild type (WT) level by introduction of one copy of the MpSOD2 gene. Taken together our data indicates functional expression of MpSod2 protein in the yeast S. cerevisiae.

Altered Phenotypes in Saccharomyces cerevisiae by Heterologous Expression of Basidiomycete Moniliophthora perniciosa SOD2 Gene

PubMed Central

Melo, Sônia C.; Santos, Regineide X.; Melgaço, Ana C.; Pereira, Alanna C. F.; Pungartnik, Cristina; Brendel, Martin

2015-01-01

Heterologous expression of a putative manganese superoxide dismutase gene (SOD2) of the basidiomycete Moniliophthora perniciosa complemented the phenotypes of a Saccharomyces cerevisiae sod2Δ mutant. Sequence analysis of the cloned M. perniciosa cDNA revealed an open reading frame (ORF) coding for a 176 amino acid polypeptide with the typical metal-binding motifs of a SOD2 gene, named MpSOD2. Phylogenetic comparison with known manganese superoxide dismutases (MnSODs) located the protein of M. perniciosa (MpSod2p) in a clade with the basidiomycete fungi Coprinopsis cinerea and Laccaria bicolor. Haploid wild-type yeast transformants containing a single copy of MpSOD2 showed increased resistance phenotypes against oxidative stress-inducing hydrogen peroxide and paraquat, but had unaltered phenotype against ultraviolet–C (UVC) radiation. The same transformants exhibited high sensitivity against treatment with the pro-mutagen diethylnitrosamine (DEN) that requires oxidation to become an active mutagen/carcinogen. Absence of MpSOD2 in the yeast sod2Δ mutant led to DEN hyper-resistance while introduction of a single copy of this gene restored the yeast wild-type phenotype. The haploid yeast wild-type transformant containing two SOD2 gene copies, one from M. perniciosa and one from its own, exhibited DEN super-sensitivity. This transformant also showed enhanced growth at 37 °C on the non-fermentable carbon source lactate, indicating functional expression of MpSod2p. The pro-mutagen dihydroethidium (DHE)-based fluorescence assay monitored basal level of yeast cell oxidative stress. Compared to the wild type, the yeast sod2Δ mutant had a much higher level of intrinsic oxidative stress, which was reduced to wild type (WT) level by introduction of one copy of the MpSOD2 gene. Taken together our data indicates functional expression of MpSod2 protein in the yeast S. cerevisiae. PMID:26039235

Epigenetic reprogramming governs EcSOD expression during human mammary epithelial cell differentiation, tumorigenesis and metastasis

PubMed Central

Teoh-Fitzgerald, ML; Fitzgerald, MP; Zhong, W; Askeland, RW; Domann, FE

2013-01-01

Expression of the antioxidant enzyme EcSOD in normal human mammary epithelial cells was not recognized until recently. Although expression of EcSOD was not detectable in non-malignant human mammary epithelial cells (HMEC) cultured in conventional two-dimensional (2D) culture conditions, EcSOD protein expression was observed in normal human breast tissues, suggesting that the 2D-cultured condition induces a repressive status of EcSOD gene expression in HMEC. With the use of laminin-enriched extracellular matrix (lrECM), we were able to detect expression of EcSOD when HMEC formed polarized acinar structures in a 3D-culture condition. Repression of the EcSOD-gene expression was again seen when the HMEC acini were sub-cultured as a monolayer, implying that lrECM-induced acinar morphogenesis is essential in EcSOD-gene activation. We have further shown the involvement of DNA methylation in regulating EcSOD expression in HMEC under these cell culture conditions. EcSOD mRNA expression was strongly induced in the 2D-cultured HMEC after treatment with a DNA methyltransferase inhibitor. In addition, epigenetic analyses showed a decrease in the degree of CpG methylation in the EcSOD promoter in the 3D versus 2D-cultured HMEC. More importantly, >80% of clinical mammary adenocarcinoma samples showed significantly decreased EcSOD mRNA and protein expression levels compared with normal mammary tissues and there is an inverse correlation between the expression levels of EcSOD and the clinical stages of breast cancer. Combined bisulfite restriction analysis analysis of some of the tumors also revealed an association of DNA methylation with the loss of EcSOD expression in vivo. Furthermore, overexpression of EcSOD inhibited breast cancer metastasis in both the experimental lung metastasis model and the syngeneic mouse model. This study suggests that epigenetic silencing of EcSOD may contribute to mammary tumorigenesis and that restoring the extracellular superoxide scavenging

Oak Dispersal Syndromes: Do Red and White Oaks Exhibit Different Dispersal Srategies?

Treesearch

Michael Steele; Peter Smallwood; William B. Terzaghi; John E. Carlson; Thomas conteras; Amy McEuen

2004-01-01

We provide an overview of the ecological and evolutionary interactions between oaks and several of their dispersal agents, and review a series of studies that demonstrate how various acorn characteristics affect feeding and caching decisions of these animals, which in turn may influence oak dispersal and establishment. We demonstrate that acorns of red oak species show...

A molecular chaperone activity of CCS restores the maturation of SOD1 fALS mutants.

PubMed

Luchinat, Enrico; Barbieri, Letizia; Banci, Lucia

2017-12-12

Superoxide dismutase 1 (SOD1) is an important metalloprotein for cellular oxidative stress defence, that is mutated in familiar variants of Amyotrophic Lateral Sclerosis (fALS). Some mutations destabilize the apo protein, leading to the formation of misfolded, toxic species. The Copper Chaperone for SOD1 (CCS) transiently interacts with SOD1 and promotes its correct maturation by transferring copper and catalyzing disulfide bond formation. By in vitro and in-cell NMR, we investigated the role of the SOD-like domain of CCS (CCS-D2). We showed that CCS-D2 forms a stable complex with zinc-bound SOD1 in human cells, that has a twofold stabilizing effect: it both prevents the accumulation of unstructured mutant SOD1 and promotes zinc binding. We further showed that CCS-D2 interacts with apo-SOD1 in vitro, suggesting that in cells CCS stabilizes mutant apo-SOD1 prior to zinc binding. Such molecular chaperone function of CCS-D2 is novel and its implications in SOD-linked fALS deserve further investigation.

Structures of the G85R Variant of SOD1 in Familial Amyotrophic Lateral Sclerosis

DOE Office of Scientific and Technical Information (OSTI.GOV)

Cao, Xiaohang; Antonyuk, Svetlana V.; Seetharaman, Sai V.

2008-07-21

Mutations in the gene encoding human copper-zinc superoxide dismutase (SOD1) cause a dominant form of the progressive neurodegenerative disease amyotrophic lateral sclerosis. Transgenic mice expressing the human G85R SOD1 variant develop paralytic symptoms concomitant with the appearance of SOD1-enriched proteinaceous inclusions in their neural tissues. The process(es) through which misfolding or aggregation of G85R SOD1 induces motor neuron toxicity is not understood. Here we present structures of the human G85R SOD1 variant determined by single crystal x-ray diffraction. Alterations in structure of the metal-binding loop elements relative to the wild type enzyme suggest a molecular basis for the metal ionmore » deficiency of the G85R SOD1 protein observed in the central nervous system of transgenic mice and in purified recombinant G85R SOD1. These findings support the notion that metal-deficient and/or disulfide-reduced mutant SOD1 species contribute to toxicity in SOD1-linked amyotrophic lateral sclerosis.« less

Molecular identification of Nocardia species using the sodA gene: Identificación molecular de especies de Nocardia utilizando el gen sodA.

PubMed

Sánchez-Herrera, K; Sandoval, H; Mouniee, D; Ramírez-Durán, N; Bergeron, E; Boiron, P; Sánchez-Saucedo, N; Rodríguez-Nava, V

2017-09-01

Currently for bacterial identification and classification the rrs gene encoding 16S rRNA is used as a reference method for the analysis of strains of the genus Nocardia. However, it does not have enough polymorphism to differentiate them at the species level. This fact makes it necessary to search for molecular targets that can provide better identification. The sod A gene (encoding the enzyme superoxide dismutase) has had good results in identifying species of other Actinomycetes. In this study the sod A gene is proposed for the identification and differentiation at the species level of the genus Nocardia. We used 41 type species of various collections; a 386 bp fragment of the sod A gene was amplified and sequenced, and a phylogenetic analysis was performed comparing the genes rrs (1171 bp), hsp 65 (401 bp), sec A1 (494 bp), gyr B (1195 bp) and rpo B (401 bp). The sequences were aligned using the Clustal X program. Evolutionary trees according to the neighbour-joining method were created with the programs Phylo_win and MEGA 6. The specific variability of the sod A genus of the genus Nocardia was analysed. A high phylogenetic resolution, significant genetic variability, and specificity and reliability were observed for the differentiation of the isolates at the species level. The polymorphism observed in the sod A gene sequence contains variable regions that allow the discrimination of closely related Nocardia species. The clear specificity, despite its small size, proves to be of great advantage for use in taxonomic studies and clinical diagnosis of the genus Nocardia.

SOD-1 expression in pig coronary arterioles is increased by exercise training.

PubMed

Rush, J W; Laughlin, M H; Woodman, C R; Price, E M

2000-11-01

Coronary arterioles of exercise-trained (EX) pigs have enhanced nitric oxide (NO.)-dependent dilation. Evidence suggests that the biological half-life of NO. depends in part on the management of the superoxide anion. The purpose of this study was to test the hypothesis that expression of cytosolic copper/zinc-dependent superoxide dismutase (SOD)-1 is increased in coronary arterioles as a result of exercise training. Male Yucatan pigs either remained sedentary (SED, n = 4) or were EX (n = 4) on a motorized treadmill for 16-20 wk. Individual coronary arterioles ( approximately 100-microm unpressurized internal diameter) were dissected and frozen. Coronary arteriole SOD-1 protein (via immunoblots) increased as a result of exercise training (2.16 +/- 0.35 times SED levels) as did SOD-1 enzyme activity (measured via inhibition of pyrogallol autooxidation; approximately 75% increase vs. SED). In addition, SOD-1 mRNA levels (measured via RT-PCR) were higher in EX arterioles (1.68 +/- 0.16 times the SED levels). There were no effects of exercise training on the levels of SOD-2 (mitochondrial), catalase, or p67(phox) proteins. Thus chronic aerobic exercise training selectively increases the levels of SOD-1 mRNA, protein, and enzymatic activity in porcine coronary arterioles. Increased SOD-1 could contribute to the enhanced NO.-dependent dilation previously observed in EX porcine coronary arterioles by improving management of superoxide in the vascular cell environment, thus prolonging the biological half-life of NO.

Implications of fALS Mutations on Sod1 Function and Oligomerization in Cell Models.

PubMed

Brasil, Aline A; Magalhães, Rayne S S; De Carvalho, Mariana D C; Paiva, Isabel; Gerhardt, Ellen; Pereira, Marcos D; Outeiro, Tiago F; Eleutherio, Elis C A

2018-06-01

Among the familial forms of amyotrophic lateral sclerosis (fALS), 20% are associated with the Cu,Zn-superoxide dismutase (Sod1). fALS is characterized by the accumulation of aggregated proteins and the increase in oxidative stress markers. Here, we used the non-invasive bimolecular fluorescence complementation (BiFC) assay in human H4 cells to investigate the kinetics of aggregation and subcellular localization of Sod1 mutants. We also studied the effect of the different Sod1 mutants to respond against oxidative stress by following the levels of reactive oxygen species (ROS) after treatment with hydrogen peroxide. Our results showed that only 30% of cells transfected with A4VSod1 showed no inclusions while for the other Sod1 mutants tested (L38V, G93A and G93C), this percentage was at least 70%. In addition, we found that 10% of cells transfected with A4VSod1 displayed more than five inclusions per cell and that A4V and G93A Sod1 formed inclusions more rapidly than L38V and G93C Sod1. Expression of WTSod1 significantly decreased the intracellular oxidation levels in comparison with expression of fALS Sod1 mutants, suggesting the mutations induce a functional impairment. All fALS mutations impaired nuclear localization of Sod1, which is important for maintaining genomic stability. Consistently, expression of WTSod1, but not of fALS Sod1 mutants, reduced DNA damage, as measured by the comet assay. Altogether, our study sheds light into the effects of fALS Sod1 mutations on inclusion formation, dynamics, and localization as well as on antioxidant response, opening novel avenues for investigating the role of fALS Sod1 mutations in pathogenesis.

Menadione triggers cell death through ROS-dependent mechanisms involving PARP activation without requiring apoptosis.

PubMed

Loor, Gabriel; Kondapalli, Jyothisri; Schriewer, Jacqueline M; Chandel, Navdeep S; Vanden Hoek, Terry L; Schumacker, Paul T

2010-12-15

Low levels of reactive oxygen species (ROS) can function as redox-active signaling messengers, whereas high levels of ROS induce cellular damage. Menadione generates ROS through redox cycling, and high concentrations trigger cell death. Previous work suggests that menadione triggers cytochrome c release from mitochondria, whereas other studies implicate the activation of the mitochondrial permeability transition pore as the mediator of cell death. We investigated menadione-induced cell death in genetically modified cells lacking specific death-associated proteins. In cardiomyocytes, oxidant stress was assessed using the redox sensor RoGFP, expressed in the cytosol or the mitochondrial matrix. Menadione elicited rapid oxidation in both compartments, whereas it decreased mitochondrial potential and triggered cytochrome c redistribution to the cytosol. Cell death was attenuated by N-acetylcysteine and exogenous glutathione or by overexpression of cytosolic or mitochondria-targeted catalase. By contrast, no protection was observed in cells overexpressing Cu,Zn-SOD or Mn-SOD. Overexpression of antiapoptotic Bcl-X(L) protected against staurosporine-induced cell death, but it failed to confer protection against menadione. Genetic deletion of Bax and Bak, cytochrome c, cyclophilin D, or caspase-9 conferred no protection against menadione-induced cell death. However, cells lacking PARP-1 showed a significant decrease in menadione-induced cell death. Thus, menadione induces cell death through the generation of oxidant stress in multiple subcellular compartments, yet cytochrome c, Bax/Bak, caspase-9, and cyclophilin D are dispensable for cell death in this model. These studies suggest that multiple redundant cell death pathways are activated by menadione, but that PARP plays an essential role in mediating each of them. Copyright © 2010 Elsevier Inc. All rights reserved.

Menadione triggers cell death through ROS-dependent mechanisms involving PARP activation without requiring apoptosis

PubMed Central

Loor, Gabriel; Kondapalli, Jyothisri; Schriewer, Jacqueline M.; Chandel, Navdeep S.; Vanden Hoek, Terry L.; Schumacker, Paul T.

2010-01-01

Low levels of reactive oxygen species (ROS) can function as redox-active signaling messengers, whereas high levels of ROS induce cellular damage. Menadione generates ROS through redox cycling, and high concentrations trigger cell death. Previous work suggests that menadione triggers cytochrome c release from mitochondria, while other studies implicate activation of the mitochondrial permeability transition poreas the mediator of cell death. We investigated menadione-induced cell death in genetically modified cells lacking specific death-associated proteins. In cardiomyocytes, oxidant stress was assessed using the redox sensor RoGFP, expressed in the cytosol or the mitochondrial matrix. Menadione elicited rapid oxidation in both compartments, while it decreased mitochondrial potential and triggered cytochrome c redistribution to the cytosol. Cell death was attenuated by N-acetyl cysteine and exogenous glutathione (GSH), or by over-expression of cytosolic or mitochondria-targeted catalase. By contrast, no protection was observed in cells over-expressing Cu, Zn-SOD or MnSOD. Over-expression of antiapoptotic Bcl-XLprotected against staurosporine-induced cell death, but it failed to confer protection against menadione. Genetic deletion of Bax and Bak, cytochrome c, cyclophilin D or caspase-9 conferred no protection against menadione-induced cell death. However, cells lacking PARP-1 showed a significant decrease in menadione-induced cell death. Thus, menadione induces cell death through the generation of oxidant stress in multiple subcellular compartments, yet cytochromec, Bax/Bak, caspase-9 and cyclophilin D are dispensable for cell death in this model. These studies suggest that multiple redundant cell death pathways are activated by menadione, but that PARP plays an essential role in mediating each of them. PMID:20937380

High lipophilicity of meta Mn(III) N-alkylpyridylporphyrin-based SOD mimics compensates for their lower antioxidant potency and makes them equally effective as ortho analogues in protecting SOD-deficient E. coli

PubMed Central

Kos, Ivan; Benov, Ludmil; Spasojević, Ivan; Rebouças, Júlio S.; Batinić-Haberle, Ines

2009-01-01

Lipophilicity/bioavailibility of Mn(III)N-alkylpyridylporphyrin-based SOD mimics has major impact on their in vivo ability to suppress oxidative stress. Meta isomers are less potent SOD mimics than ortho analogues, but are 10-fold more lipophilic and more planar. Enhanced lipophilicity contributes to their higher accumulation in cytosol of SOD-deficient E. coli, compensating for their lower potency; consequently both isomers exert similar-to-identical protection of SOD-deficient E. coli. Thus meta isomers may be as prospective therapeutics as are ortho porphyrins. PMID:19954250

Fitting Fire into Oak Management

Treesearch

Patrick Brose

2004-01-01

In the past decade, the use of prescribed fire in the mixed-oak forests of the eastern United States has markedly increased to help overcome the chronic lack of abundant, vigorous oak regeneration (Yaussy 2000). However, pre- scribed burns implemented under inappropriate circum- stances can result in failure to establish oak regeneration and/or loss of existing oak...

Foliar nutrients explain goldspotted oak borer, Agrilus auroguttatus, adult feeding preference among four California oak species

Treesearch

Yigen Chen; Tom. W. Coleman; Michael. I. Jones; Mary. L. Flint; Steven. J. Seybold

2013-01-01

Adults of the invasive goldspotted oak borer, Agrilus auroguttatus Schaeffer (Coleoptera: Buprestidae), consumed foliar weight in no-choice feeding tests of, in descending order, California black oak Quercus kelloggii Newb., Engelmann oak, Quercus engelmannii Greene, coast live oak, Quercus...

Scolopendra subspinipes mutilans attenuates neuroinflammation in symptomatic hSOD1G93A mice

PubMed Central

2013-01-01

Background Amyotrophic lateral sclerosis (ALS) is a progressive, adult-onset neurodegenerative disorder characterized by selective motor neuron death in the spinal cord, brainstem, and motor cortex. Neuroinflammation is one of several pathological causes of degenerating motor neurons and is induced by activated microglial cells and astrocytes in ALS. Scolopendra subspinipes mutilans (SSM) is utilized in traditional Chinese and Korean medicine for the treatment of a variety of diseases, such as cancer, apoplexy, and epilepsy. However, the mechanisms underlying the effects of SSM are currently unclear, even though SSM increases immune and antibiotic activity. Methods To determine the effects of SSM on symptomatic hSOD1G93A transgenic mice, SSM (2.5 μℓ/g) was injected bilaterally at the Zusanli (ST36) acupoint three times per week for two weeks. The effects of SSM treatment on anti-neuroinflammation in the brainstem and spinal cord of hSOD1G93A mice were assessed via Nissl and Fluoro-Jade B (FJB) staining, and immunohistochemistry using Iba-1, CD14, HO1, and NQO1 proteins was evaluated by Western blotting. Results In this study, we investigated whether SSM affects neuroinflammation in the spinal cord of symptomatic hSOD1G93A transgenic mice. We found that SSM treatment attenuated the loss of motor neurons and reduced the activation of microglial cells and astrocytes. Furthermore, we demonstrated that SSM administration in this animal model of ALS suppressed oxidative stress in the brainstem and spinal cord by 1.6- and 1.8-fold, respectively. Conclusions Our findings suggest that SSM, which has previously been used in complementary and alternative medicine (CAM), might also be considered as an anti-neuroinflammatory therapy for neurodegenerative diseases. PMID:24168240

Scolopendra subspinipes mutilans attenuates neuroinflammation in symptomatic hSOD1(G93A) mice.

PubMed

Cai, MuDan; Choi, Sun-Mi; Song, Bong Keun; Son, Ilhong; Kim, Sungchul; Yang, Eun Jin

2013-10-29

Amyotrophic lateral sclerosis (ALS) is a progressive, adult-onset neurodegenerative disorder characterized by selective motor neuron death in the spinal cord, brainstem, and motor cortex. Neuroinflammation is one of several pathological causes of degenerating motor neurons and is induced by activated microglial cells and astrocytes in ALS.Scolopendra subspinipes mutilans (SSM) is utilized in traditional Chinese and Korean medicine for the treatment of a variety of diseases, such as cancer, apoplexy, and epilepsy. However, the mechanisms underlying the effects of SSM are currently unclear, even though SSM increases immune and antibiotic activity. To determine the effects of SSM on symptomatic hSOD1G93A transgenic mice, SSM (2.5 μℓ/g) was injected bilaterally at the Zusanli (ST36) acupoint three times per week for two weeks. The effects of SSM treatment on anti-neuroinflammation in the brainstem and spinal cord of hSOD1G93A mice were assessed via Nissl and Fluoro-Jade B (FJB) staining, and immunohistochemistry using Iba-1, CD14, HO1, and NQO1 proteins was evaluated by Western blotting. In this study, we investigated whether SSM affects neuroinflammation in the spinal cord of symptomatic hSOD1G93A transgenic mice. We found that SSM treatment attenuated the loss of motor neurons and reduced the activation of microglial cells and astrocytes. Furthermore, we demonstrated that SSM administration in this animal model of ALS suppressed oxidative stress in the brainstem and spinal cord by 1.6- and 1.8-fold, respectively. Our findings suggest that SSM, which has previously been used in complementary and alternative medicine (CAM), might also be considered as an anti-neuroinflammatory therapy for neurodegenerative diseases.

Oak Tatters

Treesearch

Linda Haugen; Phil Marshall; Jane Cummings Carlson; Mark Vitosh; Ed Hayes

2000-01-01

Oak tatters is a relatively new condition that affects emerging oak leaves, causing them to appear lacy or tattered. It has been observed throughout the Midwestern United States, including Minnesota, Michigan, Wisconsin, Iowa, Illinois, Indiana, Ohio, and Missouri. This disorder was first reported during the 1980's in Iowa, Indiana and Ohio, but has been observed...

Distinct oxidative cleavage and modification of bovine [Cu-Zn]-SOD by an ascorbic acid/Cu(II) system: Identification of novel copper binding site on SOD molecule

PubMed Central

Uehara, Hiroshi; Luo, Shen; Aryal, Baikuntha; Levine, Rodney L.; Rao, V. Ashutosh

2016-01-01

We investigated the combined effect of ascorbate and copper [Asc/Cu(II)] on the integrity of bovine [Cu-Zn]-superoxide dismutase (bSOD1) as a model system to study the metal catalyzed oxidation (MCO) and fragmentation of proteins. We found Asc/Cu(II) mediates specific cleavage of bSOD1 and generates 12.5 and 3.2 kDa fragments in addition to oxidation/carbonylation of the protein. The effect of other tested transition metals, a metal chelator, and hydrogen peroxide on the cleavage and oxidation indicated that binding of copper to a previously unknown site on SOD1 is responsible for the Asc/Cu(II) specific cleavage and oxidation. We utilized tandem mass spectrometry to identify the specific cleavage sites of Asc/Cu(II)-treated bSOD1. Analyses of tryptic- and AspN-peptides have demonstrated the cleavage to occur at Gly31 with peptide bond breakage with Thr30 and Ser32 through diamide and α-amidation pathways, respectively. The three-dimensional structure of bSOD1 reveals the imidazole ring of His19 localized within 5 Angstrom from the α-carbon of Gly31 providing a structural basis that copper ion, most likely coordinated by His19, catalyzes the specific cleavage reaction. PMID:26872685

Distinct oxidative cleavage and modification of bovine [Cu- Zn]-SOD by an ascorbic acid/Cu(II) system: Identification of novel copper binding site on SOD molecule.

PubMed

Uehara, Hiroshi; Luo, Shen; Aryal, Baikuntha; Levine, Rodney L; Rao, V Ashutosh

2016-05-01

We investigated the combined effect of ascorbate and copper [Asc/Cu(II)] on the integrity of bovine [Cu-Zn]-superoxide dismutase (bSOD1) as a model system to study the metal catalyzed oxidation (MCO) and fragmentation of proteins. We found Asc/Cu(II) mediates specific cleavage of bSOD1 and generates 12.5 and 3.2kDa fragments in addition to oxidation/carbonylation of the protein. The effect of other tested transition metals, a metal chelator, and hydrogen peroxide on the cleavage and oxidation indicated that binding of copper to a previously unknown site on SOD1 is responsible for the Asc/Cu(II) specific cleavage and oxidation. We utilized tandem mass spectrometry to identify the specific cleavage sites of Asc/Cu(II)-treated bSOD1. Analyses of tryptic- and AspN-peptides have demonstrated the cleavage to occur at Gly31 with peptide bond breakage with Thr30 and Ser32 through diamide and α-amidation pathways, respectively. The three-dimensional structure of bSOD1 reveals the imidazole ring of His19 localized within 5Å from the α-carbon of Gly31 providing a structural basis that copper ion, most likely coordinated by His19, catalyzes the specific cleavage reaction. Published by Elsevier Inc.

Parkin Protects Against Misfolded SOD1 Toxicity by Promoting Its Aggresome Formation and Autophagic Clearance.

PubMed

Yung, Cheryl; Sha, Di; Li, Lian; Chin, Lih-Shen

2016-11-01

Mutations in Cu/Zn superoxide dismutase (SOD1) cause autosomal dominant amyotrophic lateral sclerosis (ALS), a devastating neurodegenerative disease with no effective treatment. Despite ample evidence indicating involvement of mutation-induced SOD1 protein misfolding and aggregation in ALS pathogenesis, the molecular mechanisms that control cellular management of misfolded, aggregation-prone SOD1 mutant proteins remain unclear. Here, we report that parkin, an E3 ubiquitin-protein ligase which is linked to Parkinson's disease, is a novel regulator of cellular defense against toxicity induced by ALS-associated SOD1 mutant proteins. We find that parkin mediates K63-linked polyubiquitination of SOD1 mutants in cooperation with the UbcH13/Uev1a E2 enzyme and promotes degradation of these misfolded SOD1 proteins by the autophagy-lysosome system. In response to strong proteotoxic stress associated with proteasome impairment, parkin promotes sequestration of misfolded and aggregated SOD1 proteins to form perinuclear aggresomes, regulates positioning of lysosomes around misfolded SOD1 aggresomes, and facilitates aggresome clearance by autophagy. Our findings reveal parkin-mediated cytoprotective mechanisms against misfolded SOD1 toxicity and suggest that enhancing parkin-mediated cytoprotection may provide a novel therapeutic strategy for treating ALS.

Sustaining northern red oak forests: managing oak from regeneration to canopy dominance in mature stands

Treesearch

Daniel C. Dey; Gary W. Miller; John M. Kabrick

2008-01-01

Across the range of northern red oak, managers have problems sustaining current stocking of northern red oak in forests. Oak species are adapted to frequent stand disturbances that reduce the abundance of shade tolerant competitors and control fast-growing pioneer species. A widely recommended approach to regenerating northern red oak is to develop relatively large...

Mechanisms of Enhanced Phrenic Long-Term Facilitation in SOD1G93A Rats

PubMed Central

Satriotomo, Irawan; Grebe, Ashley M.

2017-01-01

Amyotrophic lateral sclerosis (ALS) is a degenerative motor neuron disease, causing muscle paralysis and death from respiratory failure. Effective means to preserve/restore ventilation are necessary to increase the quality and duration of life in ALS patients. At disease end-stage in a rat ALS model (SOD1G93A), acute intermittent hypoxia (AIH) restores phrenic nerve activity to normal levels via enhanced phrenic long-term facilitation (pLTF). Mechanisms enhancing pLTF in end-stage SOD1G93A rats are not known. Moderate AIH-induced pLTF is normally elicited via cellular mechanisms that require the following: Gq-protein-coupled 5-HT2 receptor activation, new BDNF synthesis, and MEK/ERK signaling (the Q pathway). In contrast, severe AIH elicits pLTF via a distinct mechanism that requires the following: Gs-protein-coupled adenosine 2A receptor activation, new TrkB synthesis, and PI3K/Akt signaling (the S pathway). In end-stage male SOD1G93A rats and wild-type littermates, we investigated relative Q versus S pathway contributions to enhanced pLTF via intrathecal (C4) delivery of small interfering RNAs targeting BDNF or TrkB mRNA, and MEK/ERK (U0126) or PI3 kinase/Akt (PI828) inhibitors. In anesthetized, paralyzed and ventilated rats, moderate AIH-induced pLTF was abolished by siBDNF and UO126, but not siTrkB or PI828, demonstrating that enhanced pLTF occurs via the Q pathway. Although phrenic motor neuron numbers were decreased in end-stage SOD1G93A rats (∼30% survival; p < 0.001), BDNF and phosphorylated ERK expression were increased in spared phrenic motor neurons (p < 0.05), consistent with increased Q-pathway contributions to pLTF. Our results increase understanding of respiratory plasticity and its potential to preserve/restore breathing capacity in ALS. SIGNIFICANCE STATEMENT Since neuromuscular disorders, such as amyotrophic lateral sclerosis (ALS), end life via respiratory failure, the ability to harness respiratory motor plasticity to improve breathing

Effects of Temperature and Drought Stress on Physiological Processes Associated With Oak Decline

Treesearch

Theodor D. Leininger

1998-01-01

Oak decline is a term used to describe a sequence of events (decline syndrome) which is typically triggered by anabioticstress and subsequently involves other biotic and abiotic factors that cause the progressive deterioration and eventual death of a tree. Decline diseases lack a single causal agent, and in that way are different from diseases caused by one pathogen or...

Cherrybark Oaks From Perforated Containers Planted as Bareroots With Open-Grown Oak Bareroots

Treesearch

Kirk D. Howell

2002-01-01

Large Cherrybark oak (Q. pagoda Raf.) grown for two years (1997 and 1998) were hoedad planted in bottomlands near Columbia, South Carolina. Successful oak plantations exist from planted bareroot cherrybark oak seedlings with heights below 50 centimeters, but costly efforts were often employed to ensure success. To overcome competing vegetation,...

Tropical sod webworm (Lepidoptera: Crambidae): a pest of warm season Turfgrasses

USDA-ARS?s Scientific Manuscript database

Larvae of Herpetogramma species (commonly called webworms, sod webworms, or grass webworms) are widely distributed throughout North America, Eurasia, Australia, New Zealand, Central and South America. Tropical sod webworm Herpetogramma phaeopteralis (Guenée) larvae are among the most destructive pes...

Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS

PubMed Central

Bosco, Daryl A.; Morfini, Gerardo; Karabacak, N. Murat; Song, Yuyu; Gros-Louis, Francois; Pasinelli, Piera; Goolsby, Holly; Fontaine, Benjamin A.; Lemay, Nathan; McKenna-Yasek, Diane; Frosch, Matthew P.; Agar, Jeffery N.; Julien, Jean-Pierre; Brady, Scott T.; Brown, Robert H.

2010-01-01

Many mutations confer upon copper/zinc superoxide dismutase-1 (SOD1) one or more toxic function(s) that impair motor neuron viability and cause familial amyotrophic lateral sclerosis (FALS). Using a conformation-specific antibody that detects misfolded SOD1 (C4F6), we demonstrate that oxidized WT-SOD1 and mutant-SOD1 share a conformational epitope that is not present in normal WT-SOD1. In a subset of human sporadic ALS (SALS) cases, motor neurons in the lumbosacral spinal cord displayed striking C4F6 immunoreactivity, denoting the presence of aberrant WT-SOD1 species. Recombinant, oxidized WT-SOD1 and WT-SOD1 immunopurified from SALS tissues inhibited kinesin-based fast axonal transport in a manner similar to FALS-linked mutant SOD1. Studies here suggest that WT-SOD1 can be pathogenic in SALS and identifies an SOD1-dependent pathogenic mechanism common to FALS and SALS. PMID:20953194

Oaks and Environmental Education

Treesearch

Kay Antunez de Mayolo

1991-01-01

A number of educational projects which focus on youth awareness and involvement with California oaks have been developed during the last five years. Primarily used in urban areas where oak populations have declined, many of these programs promote seedling propagation, tree planting and help to develop student understanding of environmental issues involving oaks while...

The paleohistory of California oaks

Treesearch

Scott Mensing

2015-01-01

Oak woodlands are a fixture of California geography, yet as recently as 10,000 years ago oaks were only a minor element in the landscape. The first fossil evidence for California's oaks is in the early Miocene (~20 million years ago) when oaks were present across the west, intermixed with deciduous trees typical of eastern North America. As climate became drier,...

Relationship between precipitation and tree mortality levels in coastal California forests infested with sudden oak death

Treesearch

Brent Oblinger; Zachary Heath; Jeffrey Moore; Lisa Fischer

2013-01-01

Phytophthora ramorum has caused extensive oak (Quercus) and tanoak (Notholithocarpus densiflorus (Hook. & Arn.) Manos, Cannon & S.H. Oh) mortality in portions of the central and north coasts of California. In conjunction with stream and terrestrial surveys, aerial detection surveys have played a...

Oak Tree Planting Project

Treesearch

Sherryl L. Nives; William D. Tietje; William H. Weitkamp

1991-01-01

An Oak Tree Planting Project was conducted during 1989/90 in San Luis Obispo County by the Integrated Hardwood Range Management Program (IHRMP)/Central Coast. The local media and an IHRMP workshop were used to publicize the Planting Project and give information on the status of oaks (Quercus spp.) in California and oak planting techniques. Outreach...

Lack of TNF-alpha receptor type 2 protects motor neurons in a cellular model of amyotrophic lateral sclerosis and in mutant SOD1 mice but does not affect disease progression.

PubMed

Tortarolo, Massimo; Vallarola, Antonio; Lidonnici, Dario; Battaglia, Elisa; Gensano, Francesco; Spaltro, Gabriella; Fiordaliso, Fabio; Corbelli, Alessandro; Garetto, Stefano; Martini, Elisa; Pasetto, Laura; Kallikourdis, Marinos; Bonetto, Valentina; Bendotti, Caterina

2015-10-01

Changes in the homeostasis of tumor necrosis factor α (TNFα) have been demonstrated in patients and experimental models of amyotrophic lateral sclerosis (ALS). However, the contribution of TNFα to the development of ALS is still debated. TNFα is expressed by glia and neurons and acts through the membrane receptors TNFR1 and TNFR2, which may have opposite effects in neurodegeneration. We investigated the role of TNFα and its receptors in the selective motor neuron death in ALS in vitro and in vivo. TNFR2 expressed by astrocytes and neurons, but not TNFR1, was implicated in motor neuron loss in primary SOD1-G93A co-cultures. Deleting TNFR2 from SOD1-G93A mice, there was partial but significant protection of spinal motor neurons, sciatic nerves, and tibialis muscles. However, no improvement of motor impairment or survival was observed. Since the sciatic nerves of SOD1-G93A/TNFR2-/- mice showed high phospho-TAR DNA-binding protein 43 (TDP-43) accumulation and low levels of acetyl-tubulin, two indices of axonal dysfunction, the lack of symptom improvement in these mice might be due to impaired function of rescued motor neurons. These results indicate the interaction between TNFR2 and membrane-bound TNFα as an innovative pathway involved in motor neuron death. Nevertheless, its inhibition is not sufficient to stop disease progression in ALS mice, underlining the complexity of this pathology. We show evidence of the involvement of neuronal and astroglial TNFR2 in the motor neuron degeneration in ALS. Both concur to cause motor neuron death in primary astrocyte/spinal neuron co-cultures. TNFR2 deletion partially protects motor neurons and sciatic nerves in SOD1-G93A mice but does not improve their symptoms and survival. However, TNFR2 could be a new target for multi-intervention therapies. © 2015 International Society for Neurochemistry.

AmeriFlux US-Oho Oak Openings

DOE Data Explorer

Chen, Jiquan [University of Toledo / Michigan State University

2016-01-01

This is the AmeriFlux version of the carbon flux data for the site US-Oho Oak Openings. Site Description - The Ohio Oak Openings site is located within the Oak Openings Preserve Metropark of northwest Ohio, one of the few remaining oak woodlands/savanna/prairie complexes in the Midwest. Declared one of the "One of America's Last Great Places" by the Nature Conservancy the area consists of four main vegetation types: Oak Woodlands, Oak Savanna, Floodplain Forests and Wet Prairies. The stand surrounding the tower is mainly Oak Woodlands dominated by red, white and black oaks with a relatively abundant population of red maples indicating high soil moisture retention and a history of limited fire disturbances. Most of the area was cleared for agriculture at the time of Euro-American settlements in the mid to late-19th century. A large fraction of the cleared land was later abandoned due to the poor sandy soils. These areas reverted to Oak Savannas and in cases where fire was limited progressively made the transition to Oak Woodlands. Today patches of the forest are burned every few years as part of prescribed burning cycle to control stand density.

SOD1 oxidation and formation of soluble aggregates in yeast: Relevance to sporadic ALS development

PubMed Central

Martins, Dorival; English, Ann M.

2014-01-01

Misfolding and aggregation of copper–zinc superoxide dismutase (Sod1) are observed in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS). Mutations in Sod1 lead to familial ALS (FALS), which is a late-onset disease. Since oxidative damage to proteins increases with age, it had been proposed that oxidation of Sod1 mutants may trigger their misfolding and aggregation in FALS. However, over 90% of ALS cases are sporadic (SALS) with no obvious genetic component. We hypothesized that oxidation could also trigger the misfolding and aggregation of wild-type Sod1 and sought to confirm this in a cellular environment. Using quiescent, stationary-phase yeast cells as a model for non-dividing motor neurons, we probed for post-translational modification (PTM) and aggregation of wild-type Sod1 extracted from these cells. By size-exclusion chromatography (SEC), we isolated two populations of Sod1 from yeast: a low-molecular weight (LMW) fraction that is catalytically active and a catalytically inactive, high-molecular weight (HMW) fraction. High-resolution mass spectrometric analysis revealed that LMW Sod1 displays no PTMs but HMW Sod1 is oxidized at Cys146 and His71, two critical residues for the stability and folding of the enzyme. HMW Sod1 is also oxidized at His120, a copper ligand, which will promote loss of this catalytic metal cofactor essential for SOD activity. Monitoring the fluorescence of a Sod1-green-fluorescent-protein fusion (Sod1-GFP) extracted from yeast chromosomally expressing this fusion, we find that HMW Sod1-GFP levels increase up to 40-fold in old cells. Thus, we speculate that increased misfolding and inclusion into soluble aggregates is a consequence of elevated oxidative modifications of wild-type Sod1 as cells age. Our observations argue that oxidative damage to wild-type Sod1 initiates the protein misfolding mechanisms that give rise to SALS. PMID:24936435

Site Index Predictions for Red Oaks and White Oak in the Boston Mountains of Arkansas

Treesearch

D.L. Graney

1977-01-01

The relationship of soil and topography to site indices of northern red (Quercus rubra L. ), black (Q. uelutina Lam.) and white (Q. alba L.) oaks in the Boston Mountains indicates that white oaks should be favored for management on the finer-textured soils and on good south and west slope sites. Both red oaks and white oak could be managed on north- and east-facing...

ALS mutant SOD1 interacts with G3BP1 and affects stress granule dynamics.

PubMed

Gal, Jozsef; Kuang, Lisha; Barnett, Kelly R; Zhu, Brian Z; Shissler, Susannah C; Korotkov, Konstantin V; Hayward, Lawrence J; Kasarskis, Edward J; Zhu, Haining

2016-10-01

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease. Mutations in Cu/Zn superoxide dismutase (SOD1) are responsible for approximately 20 % of the familial ALS cases. ALS-causing SOD1 mutants display a gain-of-toxicity phenotype, but the nature of this toxicity is still not fully understood. The Ras GTPase-activating protein-binding protein G3BP1 plays a critical role in stress granule dynamics. Alterations in the dynamics of stress granules have been reported in several other forms of ALS unrelated to SOD1. To our surprise, the mutant G93A SOD1 transgenic mice exhibited pathological cytoplasmic inclusions that co-localized with G3BP1-positive granules in spinal cord motor neurons. The co-localization was also observed in fibroblast cells derived from familial ALS patient carrying SOD1 mutation L144F. Mutant SOD1, unlike wild-type SOD1, interacted with G3BP1 in an RNA-independent manner. Moreover, the interaction is specific for G3BP1 since mutant SOD1 showed little interaction with four other RNA-binding proteins implicated in ALS. The RNA-binding RRM domain of G3BP1 and two particular phenylalanine residues (F380 and F382) are critical for this interaction. Mutant SOD1 delayed the formation of G3BP1- and TIA1-positive stress granules in response to hyperosmolar shock and arsenite treatment in N2A cells. In summary, the aberrant mutant SOD1-G3BP1 interaction affects stress granule dynamics, suggesting a potential link between pathogenic SOD1 mutations and RNA metabolism alterations in ALS.

When oak ordinances fail: unaddressed issues of oak conservation

Treesearch

Rudolph H. Light; Linda E. Pedroni

2002-01-01

The mandate by the California Board of Forestry in 1993 required each of the 41 counties which have significant oak woodlands to develop programs for the ultimate protection of this resource. As of 2001, a few counties have planned for the sustainability of their oak woodlands, but some counties may not be addressing the key components that will determine the overall...

In vivo kinetic approach reveals slow SOD1 turnover in the CNS

PubMed Central

Crisp, Matthew J.; Mawuenyega, Kwasi G.; Patterson, Bruce W.; Reddy, Naveen C.; Chott, Robert; Self, Wade K.; Weihl, Conrad C.; Jockel-Balsarotti, Jennifer; Varadhachary, Arun S.; Bucelli, Robert C.; Yarasheski, Kevin E.; Bateman, Randall J.; Miller, Timothy M.

2015-01-01

Therapeutic strategies that target disease-associated transcripts are being developed for a variety of neurodegenerative syndromes. Protein levels change as a function of their half-life, a property that critically influences the timing and application of therapeutics. In addition, both protein kinetics and concentration may play important roles in neurodegeneration; therefore, it is essential to understand in vivo protein kinetics, including half-life. Here, we applied a stable isotope-labeling technique in combination with mass spectrometric detection and determined the in vivo kinetics of superoxide dismutase 1 (SOD1), mutation of which causes amyotrophic lateral sclerosis. Application of this method to human SOD1-expressing rats demonstrated that SOD1 is a long-lived protein, with a similar half-life in both the cerebral spinal fluid (CSF) and the CNS. Additionally, in these animals, the half-life of SOD1 was longest in the CNS when compared with other tissues. Evaluation of this method in human subjects demonstrated successful incorporation of the isotope label in the CSF and confirmed that SOD1 is a long-lived protein in the CSF of healthy individuals. Together, the results of this study provide important insight into SOD1 kinetics and support application of this technique to the design and implementation of clinical trials that target long-lived CNS proteins. PMID:26075819

Sod1 deficiency reduces incubation time in mouse models of prion disease.

PubMed

Akhtar, Shaheen; Grizenkova, Julia; Wenborn, Adam; Hummerich, Holger; Fernandez de Marco, Mar; Brandner, Sebastian; Collinge, John; Lloyd, Sarah E

2013-01-01

Prion infections, causing neurodegenerative conditions such as Creutzfeldt-Jakob disease and kuru in humans, scrapie in sheep and BSE in cattle are characterised by prolonged and variable incubation periods that are faithfully reproduced in mouse models. Incubation time is partly determined by genetic factors including polymorphisms in the prion protein gene. Quantitative trait loci studies in mice and human genome-wide association studies have confirmed that multiple genes are involved. Candidate gene approaches have also been used and identified App, Il1-r1 and Sod1 as affecting incubation times. In this study we looked for an association between App, Il1-r1 and Sod1 representative SNPs and prion disease incubation time in the Northport heterogeneous stock of mice inoculated with the Chandler/RML prion strain. No association was seen with App, however, significant associations were seen with Il1-r1 (P = 0.02) and Sod1 (P<0.0001) suggesting that polymorphisms at these loci contribute to the natural variation observed in incubation time. Furthermore, following challenge with Chandler/RML, ME7 and MRC2 prion strains, Sod1 deficient mice showed highly significant reductions in incubation time of 20, 13 and 24%, respectively. No differences were detected in Sod1 expression or activity. Our data confirm the protective role of endogenous Sod1 in prion disease.

In vivo kinetic approach reveals slow SOD1 turnover in the CNS.

PubMed

Crisp, Matthew J; Mawuenyega, Kwasi G; Patterson, Bruce W; Reddy, Naveen C; Chott, Robert; Self, Wade K; Weihl, Conrad C; Jockel-Balsarotti, Jennifer; Varadhachary, Arun S; Bucelli, Robert C; Yarasheski, Kevin E; Bateman, Randall J; Miller, Timothy M

2015-07-01

Therapeutic strategies that target disease-associated transcripts are being developed for a variety of neurodegenerative syndromes. Protein levels change as a function of their half-life, a property that critically influences the timing and application of therapeutics. In addition, both protein kinetics and concentration may play important roles in neurodegeneration; therefore, it is essential to understand in vivo protein kinetics, including half-life. Here, we applied a stable isotope-labeling technique in combination with mass spectrometric detection and determined the in vivo kinetics of superoxide dismutase 1 (SOD1), mutation of which causes amyotrophic lateral sclerosis. Application of this method to human SOD1-expressing rats demonstrated that SOD1 is a long-lived protein, with a similar half-life in both the cerebral spinal fluid (CSF) and the CNS. Additionally, in these animals, the half-life of SOD1 was longest in the CNS when compared with other tissues. Evaluation of this method in human subjects demonstrated successful incorporation of the isotope label in the CSF and confirmed that SOD1 is a long-lived protein in the CSF of healthy individuals. Together, the results of this study provide important insight into SOD1 kinetics and support application of this technique to the design and implementation of clinical trials that target long-lived CNS proteins.

cIAPs promote the proteasomal degradation of mutant SOD1 linked to familial amyotrophic lateral sclerosis.

PubMed

Choi, Jin Sun; Kim, Kidae; Lee, Do Hee; Cho, Sayeon; Ha, Jae Du; Park, Byoung Chul; Kim, Sunhong; Park, Sung Goo; Kim, Jeong-Hoon

2016-11-18

Although the ubiquitin-proteasome system is believed to play an important role in the pathogenesis of familial amyotrophic lateral sclerosis (FALS), caused by mutations in Cu/Zn-superoxide dismutase 1 (SOD1), the mechanism of how mutant SOD1 protein is regulated in cells is still poorly understood. Here we have demonstrated that cellular inhibitor of apoptosis proteins (cIAPs) are specifically associated with FALS-linked mutant SOD1 (mSOD1) and that this interaction promotes the ubiquitin-dependent proteasomal degradation of mutant SOD1. By utilizing cumate inducible SOD1 cells, we also showed that knock-down or pharmacologic depletion of cIAPs leads to H 2 O 2 induced cytotoxicity in mSOD1 expressing cells. Altogether, our results reveal a novel role of cIAPs in FALS-associated mutant SOD1 regulation. Copyright © 2016 Elsevier Inc. All rights reserved.

Effects of midstory removal on underplanted black oak and white oak in the western Cumberland Plateau

Treesearch

David L. Parrott; John M. Lhotka; Jeffrey W. Stringer

2011-01-01

Difficulties in successful oak regeneration have led to the examination of various techniques to increase oak recruitment. To ensure sufficient regeneration, oak seedlings can be underplanted and used in conjunction with intermediate treatments, such as midstory removal, that create a light environment favorable to oak advance reproduction. This study examines the 5-...

Calcium Ions Promote Superoxide Dismutase 1 (SOD1) Aggregation into Non-fibrillar Amyloid

PubMed Central

Leal, Sónia S.; Cardoso, Isabel; Valentine, Joan S.; Gomes, Cláudio M.

2013-01-01

Imbalance in metal ion homeostasis is a hallmark in neurodegenerative conditions involving protein deposition, and amyotrophic lateral sclerosis (ALS) is no exception. In particular, Ca2+ dysregulation has been shown to correlate with superoxide dismutase-1 (SOD1) aggregation in a cellular model of ALS. Here we present evidence that SOD1 aggregation is enhanced and modulated by Ca2+. We show that at physiological pH, Ca2+ induces conformational changes that increase SOD1 β-sheet content, as probed by far UV CD and attenuated total reflectance-FTIR, and enhances SOD1 hydrophobicity, as probed by ANS fluorescence emission. Moreover, dynamic light scattering analysis showed that Ca2+ boosts the onset of SOD1 aggregation. In agreement, Ca2+ decreases SOD1 critical concentration and nucleation time during aggregation kinetics, as evidenced by thioflavin T fluorescence emission. Attenuated total reflectance FTIR analysis showed that Ca2+ induced aggregates consisting preferentially of antiparallel β-sheets, thus suggesting a modulation effect on the aggregation pathway. Transmission electron microscopy and analysis with conformational anti-fibril and anti-oligomer antibodies showed that oligomers and amyloidogenic aggregates constitute the prevalent morphology of Ca2+-induced aggregates, thus indicating that Ca2+ diverts SOD1 aggregation from fibrils toward amorphous aggregates. Interestingly, the same heterogeneity of conformations is found in ALS-derived protein inclusions. We thus hypothesize that transient variations and dysregulation of cellular Ca2+ levels contribute to the formation of SOD1 aggregates in ALS patients. In this scenario, Ca2+ may be considered as a pathogenic effector in the formation of ALS proteinaceous inclusions. PMID:23861388

Copper Homeostasis as a Therapeutic Target in Amyotrophic Lateral Sclerosis with SOD1 Mutations

PubMed Central

Tokuda, Eiichi; Furukawa, Yoshiaki

2016-01-01

Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative disease affecting both upper and lower motor neurons, and currently, there is no cure or effective treatment. Mutations in a gene encoding a ubiquitous antioxidant enzyme, Cu,Zn-superoxide dismutase (SOD1), have been first identified as a cause of familial forms of ALS. It is widely accepted that mutant SOD1 proteins cause the disease through a gain in toxicity but not through a loss of its physiological function. SOD1 is a major copper-binding protein and regulates copper homeostasis in the cell; therefore, a toxicity of mutant SOD1 could arise from the disruption of copper homeostasis. In this review, we will briefly review recent studies implying roles of copper homeostasis in the pathogenesis of SOD1-ALS and highlight the therapeutic interventions focusing on pharmacological as well as genetic regulations of copper homeostasis to modify the pathological process in SOD1-ALS. PMID:27136532

Copper Homeostasis as a Therapeutic Target in Amyotrophic Lateral Sclerosis with SOD1 Mutations.

PubMed

Tokuda, Eiichi; Furukawa, Yoshiaki

2016-04-28

Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative disease affecting both upper and lower motor neurons, and currently, there is no cure or effective treatment. Mutations in a gene encoding a ubiquitous antioxidant enzyme, Cu,Zn-superoxide dismutase (SOD1), have been first identified as a cause of familial forms of ALS. It is widely accepted that mutant SOD1 proteins cause the disease through a gain in toxicity but not through a loss of its physiological function. SOD1 is a major copper-binding protein and regulates copper homeostasis in the cell; therefore, a toxicity of mutant SOD1 could arise from the disruption of copper homeostasis. In this review, we will briefly review recent studies implying roles of copper homeostasis in the pathogenesis of SOD1-ALS and highlight the therapeutic interventions focusing on pharmacological as well as genetic regulations of copper homeostasis to modify the pathological process in SOD1-ALS.

An Analysis of Interactions between Fluorescently-Tagged Mutant and Wild-Type SOD1 in Intracellular Inclusions

PubMed Central

Qualls, David A.; Crosby, Keith; Brown, Hilda; Borchelt, David R.

2013-01-01

Background By mechanisms yet to be discerned, the co-expression of high levels of wild-type human superoxide dismutase 1 (hSOD1) with variants of hSOD1 encoding mutations linked familial amyotrophic lateral sclerosis (fALS) hastens the onset of motor neuron degeneration in transgenic mice. Although it is known that spinal cords of paralyzed mice accumulate detergent insoluble forms of WT hSOD1 along with mutant hSOD1, it has been difficult to determine whether there is co-deposition of the proteins in inclusion structures. Methodology/Principal Findings In the present study, we use cell culture models of mutant SOD1 aggregation, focusing on the A4V, G37R, and G85R variants, to examine interactions between WT-hSOD1 and misfolded mutant SOD1. In these studies, we fuse WT and mutant proteins to either yellow or red fluorescent protein so that the two proteins can be distinguished within inclusions structures. Conclusions/Significance Although the interpretation of the data is not entirely straightforward because we have strong evidence that the nature of the fused fluorophores affects the organization of the inclusions that form, our data are most consistent with the idea that normal dimeric WT-hSOD1 does not readily interact with misfolded forms of mutant hSOD1. We also demonstrate the monomerization of WT-hSOD1 by experimental mutation does induce the protein to aggregate, although such monomerization may enable interactions with misfolded mutant SOD1. Our data suggest that WT-hSOD1 is not prone to become intimately associated with misfolded mutant hSOD1 within intracellular inclusions that can be generated in cultured cells. PMID:24391857

The Effects of Bee Venom Acupuncture on the Central Nervous System and Muscle in an Animal hSOD1G93A Mutant

PubMed Central

Cai, MuDan; Choi, Sun-Mi; Yang, Eun Jin

2015-01-01

Amyotrophic lateral sclerosis (ALS) is caused by the degeneration of lower and upper motor neurons, leading to muscle paralysis and respiratory failure. However, there is no effective drug or therapy to treat ALS. Complementary and alternative medicine (CAM), including acupuncture, pharmacopuncture, herbal medicine, and massage is popular due to the significant limitations of conventional therapy. Bee venom acupuncture (BVA), also known as one of pharmacopunctures, has been used in Oriental medicine to treat inflammatory diseases. The purpose of this study is to investigate the effect of BVA on the central nervous system (CNS) and muscle in symptomatic hSOD1G93A transgenic mice, an animal model of ALS. Our findings show that BVA at ST36 enhanced motor function and decreased motor neuron death in the spinal cord compared to that observed in hSOD1G93A transgenic mice injected intraperitoneally (i.p.) with BV. Furthermore, BV treatment at ST36 eliminated signaling downstream of inflammatory proteins such as TLR4 in the spinal cords of symptomatic hSOD1G93A transgenic mice. However, i.p. treatment with BV reduced the levels of TNF-α and Bcl-2 expression in the muscle hSOD1G93A transgenic mice. Taken together, our findings suggest that BV pharmacopuncture into certain acupoints may act as a chemical stimulant to activate those acupoints and subsequently engage the endogenous immune modulatory system in the CNS in an animal model of ALS. PMID:25781653

Free cholesterol accumulation impairs antioxidant activities and aggravates apoptotic cell death in menadione-induced oxidative injury.

PubMed

Lee, Waisin; Xu, Mingjing; Li, Yue; Gu, Yong; Chen, Jianping; Wong, Derek; Fung, Peter C W; Shen, Jiangang

2011-10-01

Although the relationship between hypercholesterolemia and oxidative stress has been extensively investigated, direct evidence regarding to the roles of cholesterol accumulation in the generations of reactive oxygen species (ROS) and apoptotic cell death under oxidative stress is lack. In this study, we investigated productions of superoxide anions (O(2)(-)) and nitric oxide (NO), and apoptotic cell death in wild type Chinese hamster ovary (CHO) cells and cholesterol accumulated CHO cells genetically and chemically. Oxidative stress was induced by menadione challenge. The results revealed that abundance of free cholesterol (FC) promoted menadione-induced O(2)(-) and NO productions. FC accumulation down-regulated eNOS expression but up-regulated NADPH oxidases, and inhibited the activities of superoxide dismutase (SOD) and catalase. Treatment of menadione increased the expressions of iNOS and qp91 phox, enhanced the activities of SOD and catalase in the wild-type CHO cells but inhibited the activity of glutathione peroxidase in the cholesterol accumulated CHO cells. Moreover, FC abundance promoted apoptotic cell death in these cells. Taken together, those results suggest that free cholesterol accumulation aggravates menadione-induced oxidative stress and exacerbates apoptotic cell death. Copyright © 2011 Elsevier Inc. All rights reserved.

Is SOD2 Ala16Val Polymorphism Associated with Migraine with Aura Phenotype?

PubMed Central

Barbanti, Piero; De Marchis, Maria Laura; Egeo, Gabriella; Aurilia, Cinzia; Fofi, Luisa; Ialongo, Cristiano; Valente, Maria Giovanna; Ferroni, Patrizia; Della-Morte, David; Guadagni, Fiorella

2015-01-01

Abstract Several studies suggest a role of oxidative stress in the physiopathology of migraine, particularly in the form with aura. In a case-control study, we investigated the association between migraine and superoxide dismutase 1 (SOD1) and superoxide dismutase 2 (SOD2) genes in a cohort of 490 consecutive unrelated Caucasian migraineurs (migraine with aura [MwA], n=107; migraine without aura [MwoA], n=246; chronic migraine [CM], n=137) and 246 healthy controls recruited at our Headache and Pain Unit and stored in the Interinstitutional Multidisciplinary BioBank (BioBIM). Migraine phenotype was carefully detailed using face-to-face interviews. We examined polymorphisms of SOD1 gene (A/C substitution—rs2234694) and SOD2 gene (C/T transition—rs4880—Ala16Val). The rs4880 TT (Val/Val) genotype was associated (p=0.042) with the presence of unilateral cranial autonomic symptoms (UAs) in MwA patients. We also found a mild correlation between SOD2 rs4880 genotype and the type of acute migraine treatment (p=0.048) in MwA patients. Our findings suggest that SOD2 is a disease-modifier gene influencing oxidative mechanisms in MwA. These observations lead to the hypothesis that SOD2 polymorphism may cause a defective control of the oxidative phenomena linked to cortical spreading depression, the neurophysiological hallmark of migraine aura, causing an overstimulation of trigeminal neurons and UAs triggering. Antioxid. Redox Signal. 22, 275–279. PMID:25295643

Oak regeneration why big is better

Treesearch

Paul P. Kormanik; Shi-Jean S. Sung; T.L. Kormanik; Stanley J. Zarnoch

1995-01-01

It is generally accepted that large preharvest advanced oak regeneration is required for maintaining a significant oak component in future stands. However, developing advanced oak regeneration on productive sites has been difficult because stand prescriptions encouraging oak regeneration are the same conditions that favor development of potentially faster growing...

Perkinsus marinus superoxide dismutase 2 (PmSOD2) localizes to single-membrane subcellular compartments

DOE Office of Scientific and Technical Information (OSTI.GOV)

Fernandez-Robledo, Jose A.; Schott, Eric J.; Vasta, Gerardo R.

2008-10-17

Perkinsus marinus (Phylum Perkinsozoa), a protozoan parasite of oysters, is considered one of the earliest diverging groups of the lineage leading to dinoflagellates. Perkinsus trophozoites are phagocytosed by oyster hemocytes, where they are likely exposed to reactive oxygen species. As part of its reactive oxygen detoxifying pathway, P. marinus possesses two iron-cofactored SOD (PmSOD1 and PmSOD2). Immunoflourescence analysis of P. marinus trophozoites and gene complementation in yeast revealed that PmSOD1 is targeted to the mitochondria. Surprisingly, although PmSOD2 is characterized by a bipartite N-terminus extension typical of plastid targeting, in preliminary immunofluorescence studies it was visualized as punctuate regions inmore » the cytoplasm that could not be assigned to any organelle. Here, we used immunogold electron microscopy to examine the subcellular localization PmSOD2 in P. marinus trophozoites. Gold grains were mostly associated with single-membrane vesicle-like structures, and eventually, localized to electron-dense, apparently amorphous material present in the lumen of a larger, unique compartment. The images suggested that PmSOD2 is targeted to small vesicles that fuse and/or discharge their content into a larger compartment, possibly the large vacuole typical of the mature trophozoites. In light of the in silico targeting prediction, the association of PmSOD2 with single-membrane compartments raises interesting questions regarding its organellar targeting, and the nature of a putative relic plastid in Perkinsus species.« less

Molecular Cloning, Characterization and Predicted Structure of a Putative Copper-Zinc SOD from the Camel, Camelus dromedarius

PubMed Central

Ataya, Farid S.; Fouad, Dalia; Al-Olayan, Ebtsam; Malik, Ajamaluddin

2012-01-01

Superoxide dismutase (SOD) is the first line of defense against oxidative stress induced by endogenous and/or exogenous factors and thus helps in maintaining the cellular integrity. Its activity is related to many diseases; so, it is of importance to study the structure and expression of SOD gene in an animal naturally exposed most of its life to the direct sunlight as a cause of oxidative stress. Arabian camel (one humped camel, Camelus dromedarius) is adapted to the widely varying desert climatic conditions that extremely changes during daily life in the Arabian Gulf. Studying the cSOD1 in C. dromedarius could help understand the impact of exposure to direct sunlight and desert life on the health status of such mammal. The full coding region of a putative CuZnSOD gene of C. dromedarius (cSOD1) was amplified by reverse transcription PCR and cloned for the first time (gene bank accession number for nucleotides and amino acids are JF758876 and AEF32527, respectively). The cDNA sequencing revealed an open reading frame of 459 nucleotides encoding a protein of 153 amino acids which is equal to the coding region of SOD1 gene and protein from many organisms. The calculated molecular weight and isoelectric point of cSOD1 was 15.7 kDa and 6.2, respectively. The level of expression of cSOD1 in different camel tissues (liver, kidney, spleen, lung and testis) was examined using Real Time-PCR. The highest level of cSOD1 transcript was found in the camel liver (represented as 100%) followed by testis (45%), kidney (13%), lung (11%) and spleen (10%), using 18S ribosomal subunit as endogenous control. The deduced amino acid sequence exhibited high similarity with Cebus apella (90%), Sus scrofa (88%), Cavia porcellus (88%), Mus musculus (88%), Macaca mulatta (87%), Pan troglodytes (87%), Homo sapiens (87%), Canis familiaris (86%), Bos taurus (86%), Pongo abelii (85%) and Equus caballus (82%). Phylogenetic analysis revealed that cSOD1 is grouped together with S. scrofa. The

Real-Time Mass Spectrometry Monitoring of Oak Wood Toasting: Elucidating Aroma Development Relevant to Oak-aged Wine Quality

NASA Astrophysics Data System (ADS)

Farrell, Ross R.; Wellinger, Marco; Gloess, Alexia N.; Nichols, David S.; Breadmore, Michael C.; Shellie, Robert A.; Yeretzian, Chahan

2015-11-01

We introduce a real-time method to monitor the evolution of oak aromas during the oak toasting process. French and American oak wood boards were toasted in an oven at three different temperatures, while the process-gas was continuously transferred to the inlet of a proton-transfer-reaction time-of-flight mass spectrometer for online monitoring. Oak wood aroma compounds important for their sensory contribution to oak-aged wine were tentatively identified based on soft ionization and molecular mass. The time-intensity profiles revealed toasting process dynamics illustrating in real-time how different compounds evolve from the oak wood during toasting. Sufficient sensitivity was achieved to observe spikes in volatile concentrations related to cracking phenomena on the oak wood surface. The polysaccharide-derived compounds exhibited similar profiles; whilst for lignin-derived compounds eugenol formation differed from that of vanillin and guaiacol at lower toasting temperatures. Significant generation of oak lactone from precursors was evident at 225 oC. Statistical processing of the real-time aroma data showed similarities and differences between individual oak boards and oak wood sourced from the different origins. This study enriches our understanding of the oak toasting process and demonstrates a new analytical approach for research on wood volatiles.

Species-specific activation of Cu/Zn SOD by its CCS copper chaperone in the pathogenic yeast Candida albicans.

PubMed

Gleason, Julie E; Li, Cissy X; Odeh, Hana M; Culotta, Valeria C

2014-06-01

Candida albicans is a pathogenic yeast of important public health relevance. Virulence of C. albicans requires a copper and zinc containing superoxide dismutase (SOD1), but the biology of C. albicans SOD1 is poorly understood. To this end, C. albicans SOD1 activation was examined in baker's yeast (Saccharomyces cerevisiae), a eukaryotic expression system that has proven fruitful for the study of SOD1 enzymes from invertebrates, plants, and mammals. In spite of the 80% similarity between S. cerevisiae and C. albicans SOD1 molecules, C. albicans SOD1 is not active in S. cerevisiae. The SOD1 appears incapable of productive interactions with the copper chaperone for SOD1 (CCS1) of S. cerevisiae. C. albicans SOD1 contains a proline at position 144 predicted to dictate dependence on CCS1. By mutation of this proline, C. albicans SOD1 gained activity in S. cerevisiae, and this activity was independent of CCS1. We identified a putative CCS1 gene in C. albicans and created heterozygous and homozygous gene deletions at this locus. Loss of CCS1 resulted in loss of SOD1 activity, consistent with its role as a copper chaperone. C. albicans CCS1 also restored activity to C. albicans SOD1 expressed in S. cerevisiae. C. albicans CCS1 is well adapted for activating its partner SOD1 from C. albicans, but not SOD1 from S. cerevisiae. In spite of the high degree of homology between the SOD1 and CCS1 molecules in these two fungal species, there exists a species-specific barrier in CCS-SOD interactions which may reflect the vastly different lifestyles of the pathogenic versus the noninfectious yeast.

Redox susceptibility of SOD1 mutants is associated with the differential response to CCS over-expression in vivo.

PubMed

Son, Marjatta; Fu, Qiao; Puttaparthi, Krishna; Matthews, Christina M; Elliott, Jeffrey L

2009-04-01

Over-expression of CCS in G93A SOD1 mice accelerates neurological disease and enhances mitochondrial pathology. We studied the effect of CCS over-expression in transgenic mice expressing G37R, G86R or L126Z SOD1 mutations in order to understand factors which influence mitochondrial dysfunction. Over-expression of CCS markedly decreased survival and produced mitochondrial vacuolation in G37R SOD1 mice but not in G86R or L126Z SOD1 mice. Moreover, CCS/G37R SOD1 spinal cord showed specific reductions in mitochondrial complex IV subunits consistent with an isolated COX deficiency, while no such reductions were detected in CCS/G86R or CCS/L126Z SOD1 mice. CCS over-expression increased the ratio of reduced to oxidized SOD1 monomers in the spinal cords of G37R SOD1 as well as G93A SOD1 mice, but did not influence the redox state of G86R or L126Z SOD1 monomers. The effects of CCS on disease are SOD1 mutation dependent and correlate with SOD1 redox susceptibility.

Dietary Manganese Modulates PCB126 Toxicity, Metal Status, and MnSOD in the Rat

PubMed Central

Wang, Bingxuan; Klaren, William D.; Wels, Brian R.; Simmons, Donald L.; Olivier, Alicia K.; Wang, Kai; Robertson, Larry W.; Ludewig, Gabriele

2016-01-01

PCB126 (3,3′,4,4′,5-pentachlorobiphenyl) is a potent aryl hydrocarbon receptor agonist and induces oxidative stress. Because liver manganese (Mn) levels decrease in response to PCB126, a Mn dietary study was designed to investigate the role of Mn in PCB126 toxicity. Male Sprague Dawley rats received diets containing 0, 10, or 150 ppm added Mn for 3 weeks, followed by a single ip injection of corn oil or PCB126 (5 µmol/kg body weight). After 2 weeks, Mn, Cu, Zn, and Fe levels in the heart, liver, and liver mitochondria, and Mn-containing superoxide dismutase (MnSOD) and metallothionein mRNA, MnSOD protein, and MnSOD activity were determined. Mn levels in liver, heart, and liver mitochondria were strongly decreased by the Mn-deficient diet. Small effects on Fe levels and a stepwise increase in MnSOD activity with dietary Mn were also visible. PCB126 caused profound changes in Cu (up), Zn, Fe, and Mn (down) in liver, but not in heart, and differing effects (Cu, Zn, and Fe up, Mn down) in liver mitochondria. Liver MnSOD and metallothionein mRNA levels and MnSOD protein were increased but MnSOD activity was decreased by PCB126. PCB126-induced liver enlargement was dose-dependently reduced with increasing dietary Mn. These changes in metals homeostasis and MnSOD activity in liver but not heart may be a/the mechanism of PCB126 liver-specific toxicity. Specifically, transport of Fenton metals (Cu, Fe) into and Mn out of the mitochondria, a probable mechanism for lower MnSOD activity, may be a/the cause of PCB126-induced oxidative stress. The role of metallothioneins needs further evaluation. Dietary Mn slightly alleviated PCB126-induced toxicities. PMID:26660635

Transcriptional and phenotypic changes in aorta and aortic valve with aging and MnSOD deficiency in mice

PubMed Central

Roos, Carolyn M.; Hagler, Michael; Zhang, Bin; Oehler, Elise A.; Arghami, Arman

2013-01-01

The purpose of this study was to characterize changes in antioxidant and age-related gene expression in aorta and aortic valve with aging, and test the hypothesis that increased mitochondrial oxidative stress accelerates age-related endothelial and aortic valve dysfunction. Wild-type (MnSOD+/+) and manganese SOD heterozygous haploinsufficient (MnSOD+/−) mice were studied at 3 and 18 mo of age. In aorta from wild-type mice, antioxidant expression was preserved, although there were age-associated increases in Nox2 expression. Haploinsufficiency of MnSOD did not alter antioxidant expression in aorta, but increased expression of Nox2. When compared with that of aorta, age-associated reductions in antioxidant expression were larger in aortic valves from wild-type and MnSOD haploinsufficient mice, although Nox2 expression was unchanged. Similarly, sirtuin expression was relatively well-preserved in aorta from both genotypes, whereas expression of SIRT1, SIRT2, SIRT3, SIRT4, and SIRT6 were significantly reduced in the aortic valve. Expression of p16ink4a, a marker of cellular senescence, was profoundly increased in both aorta and aortic valve from MnSOD+/+ and MnSOD+/− mice. Functionally, we observed comparable age-associated reductions in endothelial function in aorta from both MnSOD+/+ and MnSOD+/− mice. Interestingly, inhibition of NAD(P)H oxidase with apocynin or gp91ds-tat improved endothelial function in MnSOD+/+ mice but significantly impaired endothelial function in MnSOD+/− mice at both ages. Aortic valve function was not impaired by aging or MnSOD haploinsufficiency. Changes in antioxidant and sirtuin gene expression with aging differ dramatically between aorta and aortic valve. Furthermore, although MnSOD does not result in overt cardiovascular dysfunction with aging, compensatory transcriptional responses to MnSOD deficiency appear to be tissue specific. PMID:23997094

A practical guide to oak release.

Treesearch

Constance A. Harrington; Warren D. Devine

2006-01-01

Oregon white oak savannas and woodlands represent a biological and cultural legacy in the Pacific Northwest. Many Oregon white oak stands are deteriorating owing to invasion and eventual overtopping by Douglas-fir or other conifers. Releasing the shade-intolerant oak trees from overtopping conifers can often restore these oak stands. When planning a release operation,...

Scarlet Oak Sawfly (Pest Alert)

Treesearch

USDA Forest Service

1998-01-01

The scarlet oak sawfly, Caliroa quercuscoccineae (Dyar) skeletonizes leaves of scarlet, black, pin, and white oaks in eastern North America. It is also called the oak slug sawfly because of the fact that the larvae are covered with a coat of slime that helps them adhere to foliage.

Overexpression of CCS in G93A-SOD1 mice leads to accelerated neurological deficits with severe mitochondrial pathology.

PubMed

Son, Marjatta; Puttaparthi, Krishna; Kawamata, Hibiki; Rajendran, Bhagya; Boyer, Philip J; Manfredi, Giovanni; Elliott, Jeffrey L

2007-04-03

Cu, Zn superoxide dismutase (SOD1) has been detected within spinal cord mitochondria of mutant SOD1 transgenic mice, a model of familial ALS. The copper chaperone for SOD1 (CCS) provides SOD1 with copper, facilitates the conversion of immature apo-SOD1 to a mature holoform, and influences in yeast the cytosolic/mitochondrial partitioning of SOD1. To determine how CCS affects G93A-SOD1-induced disease, we generated transgenic mice overexpressing CCS and crossed them to G93A-SOD1 or wild-type SOD1 transgenic mice. Both CCS transgenic mice and CCS/wild-type-SOD1 dual transgenic mice are neurologically normal. In contrast, CCS/G93A-SOD1 dual transgenic mice develop accelerated neurological deficits, with a mean survival of 36 days, compared with 242 days for G93A-SOD1 mice. Immuno-EM and subcellular fractionation studies on the spinal cord show that G93A-SOD1 is enriched within mitochondria in the presence of CCS overexpression. Our results indicate that CCS overexpression in G93A-SOD1 mice produces severe mitochondrial pathology and accelerates disease course.

Effects of Shade on Blue Oak and Coast Live Oak Regeneration in California Annual Grasslands

Treesearch

Pamela C. Muick

1991-01-01

Canopy effects and annual vegetation have been shown to strongly influence oak seedling survival. From the many elements composing canopy, shade was selected for experimental manipulation. A split-plot, multifactorial experiment was designed to test whether blue oak (Quercus douglasii) and coast live oak (Q. agrifolia) could...

Sod1 Loss Induces Intrinsic Superoxide Accumulation Leading to p53-Mediated Growth Arrest and Apoptosis

PubMed Central

Watanabe, Kenji; Shibuya, Shuichi; Koyama, Hirofumi; Ozawa, Yusuke; Toda, Toshihiko; Yokote, Koutaro; Shimizu, Takahiko

2013-01-01

Oxidative damages induced by a redox imbalance cause age-related changes in cells and tissues. Superoxide dismutase (SOD) enzymes play a major role in the antioxidant system and they also catalyze superoxide radicals (O2•−). Since the loss of cytoplasmic SOD (SOD1) resulted in aging-like phenotypes in several types of mouse tissue, SOD1 is essential for the maintenance of tissue homeostasis. To clarify the cellular function of SOD1, we investigated the cellular phenotypes of Sod1-deficient fibroblasts. We demonstrated that Sod1 deficiency impaired proliferation and induced apoptosis associated with O2•− accumulation in the cytoplasm and mitochondria in fibroblasts. Sod1 loss also decreased the mitochondrial membrane potential and led to DNA damage-mediated p53 activation. Antioxidant treatments effectively improved the cellular phenotypes through suppression of both intracellular O2•− accumulation and p53 activation in Sod1-deficient fibroblasts. In vivo experiments revealed that transdermal treatment with a vitamin C derivative significantly reversed the skin thinning commonly associated with the upregulated p53 action in the skin. Our findings revealed that intrinsic O2•− accumulation promoted p53-mediated growth arrest and apoptosis as well as mitochondrial disfunction in the fibroblasts. PMID:23708100

Upland Oak Regeneration and Management

Treesearch

David L. Loftis

2004-01-01

In oak-dominated plant communities and in other communities where oaks are important, the keys to natural regeneration of upland oak components are (1) to ensure presence of competitive regeneration sources, and (2) to provide timely, sufficient release of these sources. Regeneration sources vary significantly among different types of plant communities and disturbance...

Irradiated esophageal cells are protected from radiation-induced recombination by MnSOD gene therapy.

PubMed

Niu, Yunyun; Wang, Hong; Wiktor-Brown, Dominika; Rugo, Rebecca; Shen, Hongmei; Huq, M Saiful; Engelward, Bevin; Epperly, Michael; Greenberger, Joel S

2010-04-01

Radiation-induced DNA damage is a precursor to mutagenesis and cytotoxicity. During radiotherapy, exposure of healthy tissues can lead to severe side effects. We explored the potential of mitochondrial SOD (MnSOD) gene therapy to protect esophageal, pancreatic and bone marrow cells from radiation-induced genomic instability. Specifically, we measured the frequency of homologous recombination (HR) at an integrated transgene in the Fluorescent Yellow Direct Repeat (FYDR) mice, in which an HR event can give rise to a fluorescent signal. Mitochondrial SOD plasmid/liposome complex (MnSOD-PL) was administered to esophageal cells 24 h prior to 29 Gy upper-body irradiation. Single cell suspensions from FYDR, positive control FYDR-REC, and negative control C57BL/6NHsd (wild-type) mouse esophagus, pancreas and bone marrow were evaluated by flow cytometry. Radiation induced a statistically significant increase in HR 7 days after irradiation compared to unirradiated FYDR mice. MnSOD-PL significantly reduced the induction of HR by radiation at day 7 and also reduced the level of HR in the pancreas. Irradiation of the femur and tibial marrow with 8 Gy also induced a significant increase in HR at 7 days. Radioprotection by intraesophageal administration of MnSOD-PL was correlated with a reduced level of radiation-induced HR in esophageal cells. These results demonstrate the efficacy of MnSOD-PL for suppressing radiation-induced HR in vivo.

TFE-induced local unfolding and fibrillation of SOD1: bridging the experiment and simulation studies.

PubMed

Kumar, Vijay; Prakash, Amresh; Pandey, Preeti; Lynn, Andrew M; Hassan, Md Imtaiyaz

2018-05-18

Misfolding and aggregation of Cu, Zn Superoxide dismutase (SOD1) is involved in the neurodegenerative disease, amyotrophic lateral sclerosis. Many studies have shown that metal-depleted, monomeric form of SOD1 displays substantial local unfolding dynamics and is the precursor for aggregation. Here, we have studied the structure and dynamics of different apo monomeric SOD1 variants associated with unfolding and aggregation in aqueous trifluoroethanol (TFE) through experiments and simulation. TFE induces partially unfolded β-sheet-rich extended conformations in these SOD1 variants, which subsequently develops aggregates with fibril-like characteristics. Fibrillation was achieved more easily in disulfide-reduced monomeric SOD1 when compared with wild-type and mutant monomeric SOD1. At higher concentrations of TFE, a native-like structure with the increase in α-helical content was observed. The molecular dynamics simulation results illustrate distinct structural dynamics for different regions of SOD1 variants and show uniform local unfolding of β-strands. The strands protected by the zinc-binding and electrostatic loops were found to unfold first in 20% (v/v) TFE, leading to a partial unfolding of β-strands 4, 5, and 6 which are prone to aggregation. Our results thus shed light on the role of local unfolding and conformational dynamics in SOD1 misfolding and aggregation. © 2018 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.

DJ-1 Is a Copper Chaperone Acting on SOD1 Activation*

PubMed Central

Girotto, Stefania; Cendron, Laura; Bisaglia, Marco; Tessari, Isabella; Mammi, Stefano; Zanotti, Giuseppe; Bubacco, Luigi

2014-01-01

Lack of oxidative stress control is a common and often prime feature observed in many neurodegenerative diseases. Both DJ-1 and SOD1, proteins involved in familial Parkinson disease and amyotrophic lateral sclerosis, respectively, play a protective role against oxidative stress. Impaired activity and modified expression of both proteins have been observed in different neurodegenerative diseases. A potential cooperative action of DJ-1 and SOD1 in the same oxidative stress response pathway may be suggested based on a copper-mediated interaction between the two proteins reported here. To investigate the mechanisms underlying the antioxidative function of DJ-1 in relation to SOD1 activity, we investigated the ability of DJ-1 to bind copper ions. We structurally characterized a novel copper binding site involving Cys-106, and we investigated, using different techniques, the kinetics of DJ-1 binding to copper ions. The copper transfer between the two proteins was also examined using both fluorescence spectroscopy and specific biochemical assays for SOD1 activity. The structural and functional analysis of the novel DJ-1 copper binding site led us to identify a putative role for DJ-1 as a copper chaperone. Alteration of the coordination geometry of the copper ion in DJ-1 may be correlated to the physiological role of the protein, to a potential failure in metal transfer to SOD1, and to successive implications in neurodegenerative etiopathogenesis. PMID:24567322

INSECT SPECIES ON VEGETATION OF THE WHITE OAK LAKE BED, OAK RIDGE, TENNESSEE

DOE Office of Scientific and Technical Information (OSTI.GOV)

Howden, H.F.; Crossley, D.A. Jr.

White Oak Lake, Oak Ridge, Tennessee, received lowlevel radioactive wastes from Oak Ridge National Laboratory for 12 years prior to draining in 1955. Studies on the insects inhabiting the vegetation on White Oak Lake bed revealed 401 species present during 1956 and 1957. Most numerous were members of the insect Orders Hymenoptera, Diptera, and Coleoptera. In the summer of 1956, the first summer following draining of the lake, there were relatively fewer species of insects represented by large numbers of individuals. In 1957, there were relatively more species of insects but fewer individuals were present. By the end of themore » summer of 1957, only two years after the lake was drained, the vegetation supported a rich and varied insect fauna. (C.H.)« less

Genome-Wide Identification and Transcriptional Expression Analysis of Cucumber Superoxide Dismutase (SOD) Family in Response to Various Abiotic Stresses

PubMed Central

Zhou, Yong; Hu, Lifang; Wu, Hao; Jiang, Lunwei

2017-01-01

Superoxide dismutase (SOD) proteins are widely present in the plant kingdom and play important roles in different biological processes. However, little is known about the SOD genes in cucumber. In this study, night SOD genes were identified from cucumber (Cucumis sativus) using bioinformatics-based methods, including 5 Cu/ZnSODs, 3 FeSODs, and 1 MnSOD. Gene structure and motif analysis indicated that most of the SOD genes have relatively conserved exon/intron arrangement and motif composition. Phylogenetic analyses with SODs from cucumber and several other species revealed that these SOD proteins can be traced back to two ancestral SODs before the divergence of monocot and dicot plants. Many cis-elements related to stress responses and plant hormones were found in the promoter sequence of each CsSOD gene. Gene expression analysis revealed that most of the CsSOD genes are expressed in almost all the tested tissues. qRT-PCR analysis of 8 selected CsSOD genes showed that these genes could respond to heat, cold, osmotic, and salt stresses. Our results provide a basis for further functional research on SOD gene family in cucumber and facilitate their potential applications in the genetic improvement of cucumber. PMID:28808654

Thermal fluctuations of immature SOD1 lead to separate folding and misfolding pathways

PubMed Central

Sekhar, Ashok; Rumfeldt, Jessica AO; Broom, Helen R; Doyle, Colleen M; Bouvignies, Guillaume; Meiering, Elizabeth M; Kay, Lewis E

2015-01-01

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease involving cytotoxic conformations of Cu, Zn superoxide dismutase (SOD1). A major challenge in understanding ALS disease pathology has been the identification and atomic-level characterization of these conformers. Here, we use a combination of NMR methods to detect four distinct sparsely populated and transiently formed thermally accessible conformers in equilibrium with the native state of immature SOD1 (apoSOD12SH). Structural models of two of these establish that they possess features present in the mature dimeric protein. In contrast, the other two are non-native oligomers in which the native dimer interface and the electrostatic loop mediate the formation of aberrant intermolecular interactions. Our results show that apoSOD12SH has a rugged free energy landscape that codes for distinct kinetic pathways leading to either maturation or non-native association and provide a starting point for a detailed atomic-level understanding of the mechanisms of SOD1 oligomerization. DOI: http://dx.doi.org/10.7554/eLife.07296.001 PMID:26099300

Vegetative characteristics of oak savannas in the southwestern United States: a comparative analysis with oak woodlands in the region

Treesearch

Peter F. Ffolliott; Gerald J. Gottfried

2005-01-01

Much has been learned about the oak woodlands of the Southwestern United States in recent years. However, comparable characterizations of the companion oak savannas are needed to help in enhancing the knowledge of all oak ecosystems in the Madrean Archipelago region. Oak savannas differ from oak woodlands in that they are more open in their structure with fewer trees...

In-cell NMR reveals potential precursor of toxic species from SOD1 fALS mutants

NASA Astrophysics Data System (ADS)

Luchinat, Enrico; Barbieri, Letizia; Rubino, Jeffrey T.; Kozyreva, Tatiana; Cantini, Francesca; Banci, Lucia

2014-11-01

Mutations in the superoxide dismutase 1 (SOD1) gene are related to familial cases of amyotrophic lateral sclerosis (fALS). Here we exploit in-cell NMR to characterize the protein folding and maturation of a series of fALS-linked SOD1 mutants in human cells and to obtain insight into their behaviour in the cellular context, at the molecular level. The effect of various mutations on SOD1 maturation are investigated by changing the availability of metal ions in the cells, and by coexpressing the copper chaperone for SOD1, hCCS. We observe for most of the mutants the occurrence of an unstructured SOD1 species, unable to bind zinc. This species may be a common precursor of potentially toxic oligomeric species, that are associated with fALS. Coexpression of hCCS in the presence of copper restores the correct maturation of the SOD1 mutants and prevents the formation of the unstructured species, confirming that hCCS also acts as a molecular chaperone.

Status of oak seedlings and saplings in the northern United States: implications for sustainability of oak forests

Treesearch

Chris W. Woodall; Randall S. Morin; Jim R. Steinman; Charles H. Perry

2008-01-01

Oak species are a substantial component of forest ecosystems in a 24-state region spanning the northern U.S. During recent decades, it has been documented that the health of oak forests has been experiencing large-scale decline. To further evaluate the sustainability of oak forests in nearly half the states of the U.S., the current status of oak seedlings and saplings...

The red oak - white oak forests of the Anthracite Region

Treesearch

C. F. Burnham; M. J. Ferree; F. E. Cunningham

1947-01-01

The red oak - white oak forests of the Anthracite Region occupy as substantial portion - 28.6 percent or 915,200 acres - of the region's 3,198,400 acres of forest land. These forests have been so heavily cut for lumber and mine timbers during the past 100 years and have been so badly ravaged by fire following these heavy cuttings that in their present condition...

In yeast redistribution of Sod1 to the mitochondrial intermembrane space provides protection against respiration derived oxidative stress.

PubMed

Klöppel, Christine; Michels, Christine; Zimmer, Julia; Herrmann, Johannes M; Riemer, Jan

2010-12-03

The antioxidative enzyme copper-zinc superoxide dismutase (Sod1) is an important cellular defence system against reactive oxygen species (ROS). While the majority of this enzyme is localized to the cytosol, about 1% of the cellular Sod1 is present in the intermembrane space (IMS) of mitochondria. These amounts of mitochondrial Sod1 are increased for certain Sod1 mutants that are linked to the neurodegenerative disease amyotrophic lateral sclerosis (ALS). To date, only little is known about the physiological function of mitochondrial Sod1. Here, we use the model system Saccharomyces cerevisiae to generate cells in which Sod1 is exclusively localized to the IMS. We find that IMS-localized Sod1 can functionally substitute wild type Sod1 and that it even exceeds the protective capacity of wild type Sod1 under conditions of mitochondrial ROS stress. Moreover, we demonstrate that upon expression in yeast cells the common ALS-linked mutant Sod1(G93A) becomes enriched in the mitochondrial fraction and provides an increased protection of cells from mitochondrial oxidative stress. Such an effect cannot be observed for the catalytically inactive mutant Sod1(G85R). Our observations suggest that the targeting of Sod1 to the mitochondrial IMS provides an increased protection against respiration-derived ROS. Copyright © 2010 Elsevier Inc. All rights reserved.

Goldspotted oak borer

Treesearch

M.L. Flint; M. I. Jones; T. W. Coleman; S.J. Seybold

2013-01-01

The goldspotted oak borer (GSOB), Agrilus auroguttatus (Coleoptera: Buprestidae), is a flatheaded borer introduced to San Diego County, California, in the late 1990s or early 2000s and also detected at one site in Riverside County in 2012. It was likely brought into the state on oak firewood collected and transported from the insect's native...

Manganese-superoxide dismutase (MnSOD), a role player in seahorse (Hippocampus abdominalis) antioxidant defense system and adaptive immune system.

PubMed

Perera, N C N; Godahewa, G I; Lee, Seongdo; Kim, Myoung-Jin; Hwang, Jee Youn; Kwon, Mun Gyeong; Hwang, Seong Don; Lee, Jehee

2017-09-01

Manganese superoxide dismutase (MnSOD) is a metaloenzyme that catalyzes dismutation of the hazardous superoxide radicals into less hazardous H 2 O 2 and H 2 O. Here, we identified a homolog of MnSOD from big belly seahorse (Hippocampus abdominalis; HaMnSOD) and characterized its structural and functional features. HaMnSOD transcript possessed an open reading frame (ORF) of 672 bp which codes for a peptide of 223 amino acids. Pairwise alignment showed that HaMnSOD shared highest identity with rock bream MnSOD. Results of the phylogenetic analysis of HaMnSOD revealed a close proximity with rock bream MnSOD which was consistent with the result of homology alignment. The intense expression of HaMnSOD was observed in the ovary, followed by the heart and the brain. Further, immune related responses of HaMnSOD towards pathogenic stimulation were observed through bacterial and viral challenges. Highest HaMnSOD expression in response to stimulants Edwardsiella tarda, Streptococcus iniae, lipopolysaccharide (LPS), and polyinosinic-polycytidylic acid (Poly I:C) was observed in the late stage in the blood tissue. Xanthine/xanthine oxidase assay (XOD assay) indicated the ROS-scavenging ability of purified recombinant HaMnSOD (rHaMnSOD). The optimum conditions for the SOD activity of rHaMnSOD were pH 9 and the 25 °C. Collectively, the results obtained through the expressional analysis profiles and the functional assays provide insights into potential immune related and antioxidant roles of HaMnSOD in the big belly seahorse. Copyright © 2017 Elsevier Ltd. All rights reserved.

Silvicultural methods for regenerating oaks

Treesearch

F. Bryan Clark; Richard F. Watt

1971-01-01

Advance reproduction is the key to forming the new oak stand. However, the size or strength of the advance stems is just as important as number. Most oak stands approaching maturity have enough advance reproduction, but many do not. In such cases, harvest cuttings must be delayed and overstory densities regulated to favor the establishment and development of new oaks...

The historical significance of oak

Treesearch

J. V. Thirgood

1971-01-01

A brief history of the importance of oak in Europe, contrasting the methods used in France and Britain to propagate the species and manage the forests for continued productivity. The significance of oak as a strategic resource during the sailing-ship era is stressed, and mention is made of the early development of oak management in North America. The international...

Phrenic long-term facilitation following intrapleural CTB-SAP-induced respiratory motor neuron death.

PubMed

Nichols, Nicole L; Craig, Taylor A; Tanner, Miles A

2017-08-16

Amyotrophic lateral sclerosis (ALS) is a devastating disease leading to progressive motor neuron degeneration and death by ventilatory failure. In a rat model of ALS (SOD1 G93A ), phrenic long-term facilitation (pLTF) following acute intermittent hypoxia (AIH) is enhanced greater than expected at disease end-stage but the mechanism is unknown. We suggest that one trigger for this enhancement is motor neuron death itself. Intrapleural injections of cholera toxin B fragment conjugated to saporin (CTB-SAP) selectively kill respiratory motor neurons and mimic motor neuron death observed in SOD1 G93A rats. This CTB-SAP model allows us to study the impact of respiratory motor neuron death on breathing without many complications attendant to ALS. Here, we tested the hypothesis that phrenic motor neuron death is sufficient to enhance pLTF. pLTF was assessed in anesthetized, paralyzed and ventilated Sprague Dawley rats 7 and 28days following bilateral intrapleural injections of: 1) CTB-SAP (25μg), or 2) un-conjugated CTB and SAP (control). CTB-SAP enhanced pLTF at 7 (CTB-SAP: 162±18%, n=8 vs. 63±3%; n=8; p<0.05), but not 28days post-injection (CTB-SAP: 64±10%, n=10 vs. 60±13; n=8; p>0.05). Thus, pLTF at 7 (not 28) days post-CTB-SAP closely resembles pLTF in end-stage ALS rats, suggesting that processes unique to the early period of motor neuron death enhance pLTF. This project increases our understanding of respiratory plasticity and its implications for breathing in motor neuron disease. Copyright © 2017 Elsevier B.V. All rights reserved.

Propagation of Southern Red Oak and Water Oak by Rooted Cuttings

Treesearch

Horace J. Duncan; Fred R. Matthews

1969-01-01

Southern red oak and water oak, needed in studies of fusiform rust of southern pines, were propagated from cuttings of rooted stump sprouts and mature tree branches placed in outdoor propagation beds in June. Root strike and root development were increased when cuttings with basal wounds were treated with both the hormone IBA and the fungicide folpet. Cuttings from...

Distinct roles for motor neuron autophagy early and late in the SOD1G93A mouse model of ALS

PubMed Central

Rudnick, Noam D.; Griffey, Christopher J.; Guarnieri, Paolo; Gerbino, Valeria; Wang, Xueyong; Piersaint, Jason A.; Tapia, Juan Carlos; Rich, Mark M.; Maniatis, Tom

2017-01-01

Mutations in autophagy genes can cause familial and sporadic amyotrophic lateral sclerosis (ALS). However, the role of autophagy in ALS pathogenesis is poorly understood, in part due to the lack of cell type-specific manipulations of this pathway in animal models. Using a mouse model of ALS expressing mutant superoxide dismutase 1 (SOD1G93A), we show that motor neurons form large autophagosomes containing ubiquitinated aggregates early in disease progression. To investigate whether this response is protective or detrimental, we generated mice in which the critical autophagy gene Atg7 was specifically disrupted in motor neurons (Atg7 cKO). Atg7 cKO mice were viable but exhibited structural and functional defects at a subset of vulnerable neuromuscular junctions. By crossing Atg7 cKO mice to the SOD1G93A mouse model, we found that autophagy inhibition accelerated early neuromuscular denervation of the tibialis anterior muscle and the onset of hindlimb tremor. Surprisingly, however, lifespan was extended in Atg7 cKO; SOD1G93A double-mutant mice. Autophagy inhibition did not prevent motor neuron cell death, but it reduced glial inflammation and blocked activation of the stress-related transcription factor c-Jun in spinal interneurons. We conclude that motor neuron autophagy is required to maintain neuromuscular innervation early in disease but eventually acts in a non–cell-autonomous manner to promote disease progression. PMID:28904095

The Wye Oaks on Campus | Poster

Cancer.gov

The Wye Oak tree—a towering white oak that lived for nearly 500 years in Talbot County, Maryland—was the nation’s largest white oak tree as well as the State Tree of Maryland until it was destroyed in a severe thunderstorm in 2002. Today, several clones of the Wye Oak, as well as a few of the Wye Oak’s progeny, still exist—including two on the NCI at Frederick campus.

The effect of ILLLI on peripheral blood SOD, MDA in psoriasis treatment

NASA Astrophysics Data System (ADS)

Zhu, Jing; Nie, Fan

2005-07-01

Objective: To research the effect of Intravascular low level laser irradiation (ILLLI) on the SOD,MDA in the treatment of psoriasis. Method :47 patients suffering from psoriasis from five groups were treated by Intravascular low level laser irradiation (power:4-5mw,1h per day, period of treatment: 10 days) .We checked the change of SOD,MDA peripheral blood in 10 normal people between pre and post treatment. Group A were treated by He-Ne laser combined with drug, group B were treated by semi-conductor laser combined with drug, group C were treated only by He-Ne laser, group D were treated only by semiconductor laser, group E were treated only by drug . Results: The levels of SOD in red cell of psoriatic patients from five groups after treatment were significantly lower than that of controlled group. The levels of SOD of them were significantly increased and nearly closed to that of controlled group; the levels of MDA in red cell of psoriatic patients from five groups after treatment were significantly higher than that of controlled group; the levels of MDA of them are decreased ,however, they were still not recovered to normal levels. Conclusions: ILLLI, both He-Ne laser and semiconductor laser, can activate SOD in psoriasis patients and enhance their ability of anti-oxidation.

Import, maturation, and function of SOD1 and its copper chaperone CCS in the mitochondrial intermembrane space.

PubMed

Kawamata, Hibiki; Manfredi, Giovanni

2010-11-01

Cu, Zn, superoxide dismutase (SOD1) is a ubiquitous enzyme localized in multiple cellular compartments, including mitochondria, where it concentrates in the intermembrane space (IMS). Similar to other small IMS proteins, the import and retention of SOD1 in the IMS is linked to its folding and maturation, involving the formation of critical intra- and intermolecular disulfide bonds. Therefore, the cysteine residues of SOD1 play a fundamental role in its IMS localization. IMS import of SOD1 involves its copper chaperone, CCS, whose mitochondrial distribution is regulated by the Mia40/Erv1 disulfide relay system in a redox-dependent manner: CCS promotes SOD1 maturation and retention in the IMS. The function of SOD1 in the IMS is still unknown, but it is plausible that it serves to remove superoxide released from the mitochondrial respiratory chain. Mutations in SOD1 cause familial amyotrophic lateral sclerosis (ALS), whose pathologic features include mitochondrial bioenergetic dysfunction. Mutant SOD1 localization in the IMS is not dictated by oxygen concentration and the Mia40/Erv1 system, but is primarily dependent on aberrant protein folding and aggregation. Mutant SOD1 localization and aggregation in the IMS might cause the mitochondrial abnormalities observed in familial ALS and could play a significant role in disease pathogenesis.

Purple martins in oak woodlands

Treesearch

Brian D. C. Williams

2002-01-01

Purple martins are cavity-nesting swallows that once nested fairly widely in California’s oak woodlands but are now rare in that habitat. The old oaks of the Tehachapi Range (southern Sierra Nevada) may now host the last martins that nest in oak woodlands, with approximately 100-200 pairs or about 15 percent of the California population. In summer of 2000, we found 57...

Size and targeting to PECAM vs ICAM control endothelial delivery, internalization and protective effect of multimolecular SOD conjugates.

PubMed

Shuvaev, Vladimir V; Muro, Silvia; Arguiri, Evguenia; Khoshnejad, Makan; Tliba, Samira; Christofidou-Solomidou, Melpo; Muzykantov, Vladimir R

2016-07-28

Controlled endothelial delivery of SOD may alleviate abnormal local surplus of superoxide involved in ischemia-reperfusion, inflammation and other disease conditions. Targeting SOD to endothelial surface vs. intracellular compartments is desirable to prevent pathological effects of external vs. endogenous superoxide, respectively. Thus, SOD conjugated with antibodies to cell adhesion molecule PECAM (Ab/SOD) inhibits pro-inflammatory signaling mediated by endogenous superoxide produced in the endothelial endosomes in response to cytokines. Here we defined control of surface vs. endosomal delivery and effect of Ab/SOD, focusing on conjugate size and targeting to PECAM vs. ICAM. Ab/SOD enlargement from about 100 to 300nm enhanced amount of cell-bound SOD and protection against extracellular superoxide. In contrast, enlargement inhibited endocytosis of Ab/SOD and diminished mitigation of inflammatory signaling of endothelial superoxide. In addition to size, shape is important: endocytosis of antibody-coated spheres was more effective than that of polymorphous antibody conjugates. Further, targeting to ICAM provides higher endocytic efficacy than targeting to PECAM. ICAM-targeted Ab/SOD more effectively mitigated inflammatory signaling by intracellular superoxide in vitro and in animal models, although total uptake was inferior to that of PECAM-targeted Ab/SOD. Therefore, both geometry and targeting features of Ab/SOD conjugates control delivery to cell surface vs. endosomes for optimal protection against extracellular vs. endosomal oxidative stress, respectively. Copyright © 2016 Elsevier B.V. All rights reserved.

Genetic disruption of SOD1 gene causes glucose intolerance and impairs β-cell function.

PubMed

Muscogiuri, Giovanna; Salmon, Adam B; Aguayo-Mazzucato, Cristina; Li, Mengyao; Balas, Bogdan; Guardado-Mendoza, Rodolfo; Giaccari, Andrea; Reddick, Robert L; Reyna, Sara M; Weir, Gordon; Defronzo, Ralph A; Van Remmen, Holly; Musi, Nicolas

2013-12-01

Oxidative stress has been associated with insulin resistance and type 2 diabetes. However, it is not clear whether oxidative damage is a cause or a consequence of the metabolic abnormalities present in diabetic subjects. The goal of this study was to determine whether inducing oxidative damage through genetic ablation of superoxide dismutase 1 (SOD1) leads to abnormalities in glucose homeostasis. We studied SOD1-null mice and wild-type (WT) littermates. Glucose tolerance was evaluated with intraperitoneal glucose tolerance tests. Peripheral and hepatic insulin sensitivity was quantitated with the euglycemic-hyperinsulinemic clamp. β-Cell function was determined with the hyperglycemic clamp and morphometric analysis of pancreatic islets. Genetic ablation of SOD1 caused glucose intolerance, which was associated with reduced in vivo β-cell insulin secretion and decreased β-cell volume. Peripheral and hepatic insulin sensitivity were not significantly altered in SOD1-null mice. High-fat diet caused glucose intolerance in WT mice but did not further worsen the glucose intolerance observed in standard chow-fed SOD1-null mice. Our findings suggest that oxidative stress per se does not play a major role in the pathogenesis of insulin resistance and demonstrate that oxidative stress caused by SOD1 ablation leads to glucose intolerance secondary to β-cell dysfunction.

Genetic Disruption of SOD1 Gene Causes Glucose Intolerance and Impairs β-Cell Function

PubMed Central

Muscogiuri, Giovanna; Salmon, Adam B.; Aguayo-Mazzucato, Cristina; Li, Mengyao; Balas, Bogdan; Guardado-Mendoza, Rodolfo; Giaccari, Andrea; Reddick, Robert L.; Reyna, Sara M.; Weir, Gordon; DeFronzo, Ralph A.; Van Remmen, Holly; Musi, Nicolas

2013-01-01

Oxidative stress has been associated with insulin resistance and type 2 diabetes. However, it is not clear whether oxidative damage is a cause or a consequence of the metabolic abnormalities present in diabetic subjects. The goal of this study was to determine whether inducing oxidative damage through genetic ablation of superoxide dismutase 1 (SOD1) leads to abnormalities in glucose homeostasis. We studied SOD1-null mice and wild-type (WT) littermates. Glucose tolerance was evaluated with intraperitoneal glucose tolerance tests. Peripheral and hepatic insulin sensitivity was quantitated with the euglycemic-hyperinsulinemic clamp. β-Cell function was determined with the hyperglycemic clamp and morphometric analysis of pancreatic islets. Genetic ablation of SOD1 caused glucose intolerance, which was associated with reduced in vivo β-cell insulin secretion and decreased β-cell volume. Peripheral and hepatic insulin sensitivity were not significantly altered in SOD1-null mice. High-fat diet caused glucose intolerance in WT mice but did not further worsen the glucose intolerance observed in standard chow–fed SOD1-null mice. Our findings suggest that oxidative stress per se does not play a major role in the pathogenesis of insulin resistance and demonstrate that oxidative stress caused by SOD1 ablation leads to glucose intolerance secondary to β-cell dysfunction. PMID:24009256

The structure of the Caenorhabditis elegans manganese superoxide dismutase MnSOD-3-azide complex

DOE PAGES

Hunter, Gary J.; Trinh, Chi H.; Bonetta, Rosalin; ...

2015-08-27

C. elegans MnSOD-3 has been implicated in the longevity pathway and its mechanism of catalysis is relevant to the aging process and carcinogenesis. The structures of MnSOD-3 provide unique crystallographic evidence of a dynamic region of the tetrameric interface (residues 41–54). We have determined the structure of the MnSOD-3-azide complex to 1.77-Å resolution. The analysis of this complex shows that the substrate analog, azide, binds end-on to the manganese center as a sixth ligand and that it ligates directly to a third and new solvent molecule also positioned within interacting distance to the His30 and Tyr34 residues of the substratemore » access funnel. This is the first structure of a eukaryotic MnSOD-azide complex that demonstrates the extended, uninterrupted hydrogen-bonded network that forms a proton relay incorporating three outer sphere solvent molecules, the substrate analog, the gateway residues, Gln142, and the solvent ligand. This configuration supports the formation and release of the hydrogen peroxide product in agreement with the 5-6-5 catalytic mechanism for MnSOD. The high product dissociation constant k₄ of MnSOD-3 reflects low product inhibition making this enzyme efficient even at high levels of superoxide.« less

Adaptation to chronic MG132 reduces oxidative toxicity by a CuZnSOD-dependent mechanism

PubMed Central

Leak, Rehana K.; Zigmond, Michael J.; Liou, Anthony K. F.

2010-01-01

To study whether and how cells adapt to chronic cellular stress, we exposed PC12 cells to the proteasome inhibitor MG132 (0.1 μM) for 2 weeks and longer. This treatment reduced chymotrypsin-like proteasome activity by 47% and was associated with protection against both 6-hydroxydopamine (6-OHDA, 100 μM) and higher dose MG132 (40 μM). Protection developed slowly over the course of the first 2 weeks of exposure and was chronic thereafter. There was no change in total glutathione levels after MG132. Buthionine sulfoximine (100 μM) reduced glutathione levels by 60%, but exacerbated 6-OHDA toxicity to the same extent in both MG132-treated and control cells and failed to reduce MG132-induced protection. Chronic MG132 resulted in elevated antioxidant proteins CuZn superoxide dismutase (SOD, +55%), MnSOD (+21%), and catalase (+15%), as well as chaperone heat shock protein 70 (+42%). Examination of SOD enzyme activity revealed higher levels of CuZnSOD (+40%), with no change in MnSOD. We further assessed the mechanism of protection by reducing CuZnSOD levels with two independent siRNA sequences, both of which successfully attenuated protection against 6-OHDA. Previous reports suggested that artificial overexpression of CuZnSOD in dopaminergic cells is protective. Our data complement such observations, revealing that dopaminergic cells are also able to use endogenous CuZnSOD in self-defensive adaptations to chronic stress, and that they can even do so in the face of extensive glutathione loss. PMID:18466318

Insect-oak interactions with coast live oak (Quercus agrifolia) and Engelmann oak (Q. engelmannii) at the acorn and seedling stage

Treesearch

Connell E. Dunning; Timothy D. Paine; Richard A. Redak

2002-01-01

We determined the impact of insects on both acorns and seedlings of coast live oak (Quercus agrifolia Nee) and Engelmann oak (Quercus engelmannii E. Greene). Our goals were to (1) identify insects feeding on acorns and levels of insect damage, and (2) measure performance and preference of a generalist leaf-feeding insect herbivore...

How to Distinguish Oak LEAFTIERS From LEAFROLLERS

Treesearch

Parker Snowden

1990-01-01

Oak leaftiers and oak leafrollers defoliate oaks throughout the northeastern United States and adjoining Canadian provinces. In recent years, scattered but severe outbreaks of oak leaftier have occurred in Connecticut, Massachusetts, New Jersey, New York, Pennsylvania, and West Virginia. In 1978 more than 100,000 acres were defoliated in these states....

Oak mortality risk factors and mortality estimation

Treesearch

Stephen R. Shifley; Zhaofei Fan; John M. Kabrick; Randy G. Jensen

2006-01-01

Managers are often concerned about oak mortality in maturing mixed-oak forests, but they often lack explicit information about mortality risk for oaks that differ in species, size, crown class, competitive status, and growth rate. In eastern North America, tree species in the red oak group (Quercus Section Lobatae) are typically...

The Physiology and Biochemistry of Desiccating White Oak and Cherrybark Oak Acorns

Treesearch

Kristina F. Connor; Sharon Sowa

2004-01-01

The recalcitrant behavior of white oak (Quercus alba L.) and cherrybark oak (Q. pagoda Raf.) acorns was examined in terms of effects of moisture content on seed longevity, viability, and biochemistry. Acorns of both species were fully hydrated and then subjected to drying under ambient conditions of temperature and relative...

Exposure of Mn and FeSODs, but not Cu/ZnSOD, to NO leads to nitrosonium and nitroxyl ions generation which cause enzyme modification and inactivation: an in vitro study.

PubMed

Niketíc, V; Stojanović, S; Nikolić, A; Spasić, M; Michelson, A M

1999-11-01

The effect of NO treatment in vitro on structural and functional alterations of Cu/Zn, Mn, and Fe type of SODs was studied. Significant difference in response to NO of Cu/ZnSOD compared to the Mn and Fe types was demonstrated. Cu/ZnSOD was shown to be stable with respect to NO: even on prolonged exposure, NO produced negligible effect on its structure and activity. In contrast, both Mn and Fe types were found to be NO-sensitive: exposure to NO led to their fast and extensive inactivation, which was accompanied by extensive structural alterations, including (in some of the samples tested) the cleavage of enzyme polypeptide chains, presumably at His residues of the enzyme metal binding sites. The generation of nitrosonium (NO+) and nitroxyl (NO-) ions in NO treated Mn and FeSODs, which produce enzyme modifications and inactivation, was demonstrated. The physiological and biomedical significance of described findings is briefly discussed.

Change in soil quality due to grazing and oak tree removal in California blue oak woodlands

Treesearch

Trina J. Camping; Randy A. Dahlgren; Kenneth W. Tate; William R. Horwath

2002-01-01

The effects of grazing and oak tree removal on soil quality and fertility were examined in a blue oak (Quercus douglasii) woodland in the northern Sierra Nevada foothills. Low to moderate grazing intensity has little affect on soil quality; however, oak tree removal resulted in a decrease in most soil quality parameters investigated (carbon, nitrogen...

HOW to Distinguish Oak LEAFTIERS From LEAFROLLERS

Treesearch

Parker Snowden

1990-01-01

Oak leaftiers and oak leafrollers defoliate oaks throughout the northeastern United States and adjoining Canadian provinces. In recent years, scattered but severe outbreaks of oak Leaftier have occurred in Connecticut, Massachusetts, New Jersey, New York, Pennsylvania, and West Virginia. In 1978 more than 100,000 acres were defoliated in these states. Outbreaks of the...

Pyrimethamine significantly lowers cerebrospinal fluid Cu/Zn superoxide dismutase in amyotrophic lateral sclerosis patients with SOD1 mutations.

PubMed

Lange, Dale J; Shahbazi, Mona; Silani, Vincenzo; Ludolph, Albert C; Weishaupt, Jochen H; Ajroud-Driss, Senda; Fields, Kara G; Remanan, Rahul; Appel, Stanley H; Morelli, Claudia; Doretti, Alberto; Maderna, Luca; Messina, Stefano; Weiland, Ulrike; Marklund, Stefan L; Andersen, Peter M

2017-06-01

Cu/Zn superoxide dismutase (SOD1) reduction prolongs survival in SOD1-transgenic animal models. Pyrimethamine produces dose-dependent SOD1 reduction in cell culture systems. A previous phase 1 trial showed pyrimethamine lowers SOD1 levels in leukocytes in patients with SOD1 mutations. This study investigated whether pyrimethamine lowered SOD1 levels in the cerebrospinal fluid (CSF) in patients carrying SOD1 mutations linked to familial amyotrophic lateral sclerosis (fALS/SOD1). A multicenter (5 sites), open-label, 9-month-duration, dose-ranging study was undertaken to determine the safety and efficacy of pyrimethamine to lower SOD1 levels in the CSF in fALS/SOD1. All participants underwent 3 lumbar punctures, blood draw, clinical assessment of strength, motor function, quality of life, and adverse effect assessments. SOD1 levels were measured in erythrocytes and CSF. Pyrimethamine was measured in plasma and CSF. Appel ALS score, ALS Functional Rating Scale-Revised, and McGill Quality of Life Single-Item Scale were measured at screening, visit 6, and visit 9. We enrolled 32 patients; 24 completed 6 visits (18 weeks), and 21 completed all study visits. A linear mixed effects model showed a significant reduction in CSF SOD1 at visit 6 (p < 0.001) with a mean reduction of 13.5% (95% confidence interval [CI] = 8.4-18.5) and at visit 9 (p < 0.001) with a mean reduction of 10.5% (95% CI = 5.2-15.8). Pyrimethamine is safe and well tolerated in ALS. Pyrimethamine is capable of producing a significant reduction in total CSF SOD1 protein content in patients with ALS caused by different SOD1 mutations. Further long-term studies are warranted to assess clinical efficacy. Ann Neurol 2017;81:837-848. © 2017 The Authors. Annals of Neurology published by Wiley Periodicals, Inc. on behalf of American Neurological Association.

A Crown Cover Chart for Oak Savannas

Treesearch

Jay Law; Paul Johnson; Gary Houf

1994-01-01

Although oak savannas have been defined in many ways, they are characterized by scattered trees, largely comprised of oaks, and a sparse ground layer rich in grasses and forbs (Haney and Apfelbaum 1990). Nuzzo (1986, p. 11) more specifically defined oak savannas as plant communities "...dominated by oaks having between 10 and 80 percent canopy, with or without a...

Quercus kelloggii Newb., California black oak

Treesearch

P.M. McDonald

1990-01-01

California black oak (Quercus kelloggii) exceeds all other California oaks in volume, distribution, and altitudinal range. Yet this deciduous hardwood has had little sustained commercial use and almost no management, even though its wood closely resembles that of its valuable, managed, and heavily used counterpart-northern red oak (...

Five southern California oaks: identification and postfire management

Treesearch

Timothy R. Plumb; Anthony P. Gomez

1983-01-01

Oak trees in California are subject to periodic burning by fire, but their trunks and crowns vary in tolerance to fire. And once burned, oaks are difficult to identify by species. Fifteen oak species grow in California. This report provides keys to identifying five species of southern California oaks: coast live oak (Quercus agrifolia Née...

Acute intermittent hypoxia induced phrenic long-term facilitation despite increased SOD1 expression in a rat model of ALS

PubMed Central

Nichols, Nicole L.; Satriotomo, Irawan; Harrigan, Daniel J.; Mitchell, Gordon S.

2015-01-01

Amyotrophic lateral sclerosis (ALS) is a progressive and fatal neurodegenerative disease characterized by motor neuron death. Since most ALS patients succumb to ventilatory failure from loss of respiratory motor neurons, any effective ALS treatment must preserve and/or restore breathing capacity. In rats over-expressing mutated superoxide dismutase-1 (SOD1G93A), the capacity to increase phrenic motor output is decreased at disease end-stage, suggesting imminent ventilatory failure. Acute intermittent hypoxia (AIH) induces phrenic long-term facilitation (pLTF), a form of spinal respiratory motor plasticity with potential to restore phrenic motor output in clinical disorders that compromise breathing. Since pLTF requires NADPH oxidase activity and reactive oxygen species (ROS) formation, it is blocked by NADPH oxidase inhibition and SOD mimetics in normal rats. Thus, we hypothesized that SOD1G93A (mutant; MT) rats do not express AIH-induced pLTF due to over-expression of active mutant superoxide dismutase-1. AIH-induced pLTF and hypoglossal (XII) LTF were assessed in young, pre-symptomatic and end-stage anesthetized MT rats and age-matched wild-type littermates. Contrary to predictions, pLTF and XII LTF were observed in MT rats at all ages; at end-stage, pLTF was actually enhanced. SOD1 levels were elevated in young and pre-symptomatic MT rats, yet superoxide accumulation in putative phrenic motor neurons (assessed with dihydroethidium) was unchanged; however, superoxide accumulation significantly decreased at end-stage. Thus, compensatory mechanisms appear to maintain ROS homoeostasis until late in disease progression, preserving AIH-induced respiratory plasticity. Following intrathecal injections of an NADPH oxidase inhibitor (apocynin; 600µM; 12µL), pLTF was abolished in pre-symptomatic, but not end-stage MT rats, demonstrating that pLTF is NADPH oxidase dependent in pre-symptomatic, but NADPH oxidase independent in end-stage MT rats. Mechanisms preserving

Effect of acorn moisture content at sowing on germination and seedling growth of white oak and northern red oak

Treesearch

Shi-Jean Susana Sung; Paul P. Kormanik; Catharine D. Cook; Stanley J. Zarnoch; Taryn L. Kormanik

2006-01-01

White oak (Quercus alba L.) and northern red oak (Q. rubra L.) acorns were collected locally or from seed orchards in October 2002. Mean acorn moisture content (MC) was 48 percent for white oak and 39 percent for northern red oak. These acorns were air dried to different MCs before being sown into nursery beds in early December...

Restoring Native California Oaks on Grazed Rangelands

Treesearch

Douglas D. McCreary; Jerry Tecklin

2005-01-01

Efforts to regenerate oaks on California’s oak woodlands often must address how to establish seedlings in areas grazed by livestock. Research indicates that damage to young oak seedlings from cattle varies by season, with less damage during the winter when deciduous oaks do not have leaves. While exclusion of cattle from planted areas does result in reduced damage, the...

Developing a stand hazard index for oak decline in upland Oak forests of the Ozark Highlands, Missouri

Treesearch

Fan Zhaofei; Fan Xiuli; Martin A. Spetich; Stephen R. Shifley; W. Keith Moser; Randy G. Jensen; John M. Kabrick

2011-01-01

Black oak (Quercus velutina Lam.) and scarlet oak (Quercus coccinea Muenchh.)--two major components (44% of total stand basal area) of upland oak forests--are suffering severe decline and mortality in the Ozark Highlands, Missouri. However, factors influencing their survival (mortality) are not well understood. In this study we...

Oak savanna restoration: Oak response to fire and thinning through 28 years

Treesearch

Ronald E. Masters; Jack R. Waymire

2012-01-01

We used a small plot study on Pushmataha Wildlife Management Area in southeast Oklahoma to determine the efficacy of fire frequency and thinning as management tools for restoration of oak savanna, oak woodlands, pine-bluestem woodlands, and pine savanna for application on a landscape scale. On selected experimental units, we initially reduced stand density to favor...

Fire effects in northeastern forests: oak.

Treesearch

Cary Rouse

1986-01-01

Effects of fire on the oak timber type are reviewed. Many oak stands of today originated under severe fire regimes. Fire can ill or injure oak trees. Factors determining direct injury or mortality from fire include: season of year; bark characteristics; size, vigor and form of tree; fire characteristics and stocking level.

Conifer encroachment in California oak woodlands

Treesearch

Matthew I. Cocking; J. Morgan Varner; Eamon A. Engber

2015-01-01

California deciduous oak woodlands provide many ecological, cultural, and economic benefits, and often represent unique plant communities that harbor native rare and declining species. Oak woodlands have suffered substantial losses in area and ecological integrity in the post-settlement era due to land conversion and widespread fire exclusion. Remnant oak woodlands in...

An oak wilt primer

Treesearch

Jennifer Juzwik

2000-01-01

Oak wilt, caused by the fungus Ceratocystis fagacearum {Bretz} Hunt, is an important disease of oaks (Quercus spp.) in the eastern United States. the disease occurs in 22 states and is considered the most important forest disease problem in Illinois, Iowa, Minnesota, Texas and Wisconsin. The pathogen causes mortality of thousands...

Variations in juvenile oak

Treesearch

Peter W. Garrett; Harry C. Kettlewood

1975-01-01

Data from research on 13-year-old trees in an oak planting in southeastern Pennsylvania indicate that survival and growth are not correlated with source latitude within all species tested. A complete listing of species and seed origins, along with performance of progenies, is presented for persons interested in oak improvement.

Reconstituted products from oak

Treesearch

W. C. Lewis; B. G. Heebink

1971-01-01

"Reconstituted" describes a family of panel products made from fractionated oak, bonded with either a synthetic resin or a natural lignin bond. Several current commercial fiber panel products from oak are described, and the status of research on experimental products and processes is presented. Recent technological developments are removing the stigma...

California oaks: a bibliography

Treesearch

James R. Griffin; Philip M. McDonald; Pamela C. Muick

1987-01-01

Among natural resource professionals, California oaks continue to attract considerable attention. This report provides a comprehensive bibliography of the extensive but scattered oak literature. The 768 references are organized into two systems: (a) a topical outline, in which references are displayed under key word headings and subheadings, and author-date entries...

Molecular cloning and characterization of Siamese crocodile (Crocodylus siamensis) copper, zinc superoxide dismutase (CSI-Cu,Zn-SOD) gene.

PubMed

Sujiwattanarat, Penporn; Pongsanarakul, Parinya; Temsiripong, Yosapong; Temsiripong, Theeranan; Thawornkuno, Charin; Uno, Yoshinobu; Unajak, Sasimanas; Matsuda, Yoichi; Choowongkomon, Kiattawee; Srikulnath, Kornsorn

2016-01-01

Superoxide dismutase (SOD, EC 1.15.1.1) is an antioxidant enzyme found in all living cells. It regulates oxidative stress by breaking down superoxide radicals to oxygen and hydrogen peroxide. A gene coding for Cu,Zn-SOD was cloned and characterized from Siamese crocodile (Crocodylus siamensis; CSI). The full-length expressed sequence tag (EST) of this Cu,Zn-SOD gene (designated as CSI-Cu,Zn-SOD) contained 462bp encoding a protein of 154 amino acids without signal peptides, indicated as intracellular CSI-Cu,Zn-SOD. This agreed with the results from the phylogenetic tree, which indicated that CSI-Cu,Zn-SOD belonged to the intracellular Cu,Zn-SOD. Chromosomal location determined that the CSI-Cu,Zn-SOD was localized to the proximal region of the Siamese crocodile chromosome 1p. Several highly conserved motifs, two conserved signature sequences (GFHVHEFGDNT and GNAGGRLACGVI), and conserved amino acid residues for binding copper and zinc (His(47), His(49), His(64), His(72), His(81), Asp(84), and His(120)) were also identified in CSI-Cu,Zn-SOD. Real-time PCR analysis showed that CSI-Cu,Zn-SOD mRNA was expressed in all the tissues examined (liver, pancreas, lung, kidney, heart, and whole blood), which suggests a constitutively expressed gene in these tissues. Expression of the gene in Escherichia coli cells followed by purification yielded a recombinant CSI-Cu,Zn-SOD, with Km and Vmax values of 6.075mM xanthine and 1.4×10(-3)mmolmin(-1)mg(-1), respectively. This Vmax value was 40 times lower than native Cu,Zn-SOD (56×10(-3)mmolmin(-1)mg(-1)), extracted from crocodile erythrocytes. This suggests that cofactors, protein folding properties, or post-translational modifications were lost during the protein purification process, leading to a reduction in the rate of enzyme activity in bacterial expression of CSI-Cu,Zn-SOD. Copyright © 2015 Elsevier Inc. All rights reserved.

Molecular chaperone mediated late-stage neuroprotection in the SOD1(G93A) mouse model of amyotrophic lateral sclerosis.

PubMed

Novoselov, Sergey S; Mustill, Wendy J; Gray, Anna L; Dick, James R; Kanuga, Naheed; Kalmar, Bernadett; Greensmith, Linda; Cheetham, Michael E

2013-01-01

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the selective loss of motor neurons in the spinal cord, brain stem, and motor cortex. Mutations in superoxide dismutase (SOD1) are associated with familial ALS and lead to SOD1 protein misfolding and aggregation. Here we show that the molecular chaperone, HSJ1 (DNAJB2), mutations in which cause distal hereditary motor neuropathy, can reduce mutant SOD1 aggregation and improve motor neuron survival in mutant SOD1 models of ALS. Overexpression of human HSJ1a (hHSJ1a) in vivo in motor neurons of SOD1(G93A) transgenic mice ameliorated disease. In particular, there was a significant improvement in muscle force, increased motor unit number and enhanced motor neuron survival. hHSJ1a was present in a complex with SOD1(G93A) and led to reduced SOD1 aggregation at late stages of disease progression. We also observed altered ubiquitin immunoreactivity in the double transgenic animals, suggesting that ubiquitin modification might be important for the observed improvements. In a cell model of SOD1(G93A) aggregation, HSJ1a preferentially bound to mutant SOD1, enhanced SOD1 ubiquitylation and reduced SOD1 aggregation in a J-domain and ubiquitin interaction motif (UIM) dependent manner. Collectively, the data suggest that HSJ1a acts on mutant SOD1 through a combination of chaperone, co-chaperone and pro-ubiquitylation activity. These results show that targeting SOD1 protein misfolding and aggregation in vivo can be neuroprotective and suggest that manipulation of DnaJ molecular chaperones might be useful in the treatment of ALS.

Reducing borer damage in oak regeneration and sawtimber

Treesearch

Jimmy R. Galford

1989-01-01

Borers cause millions of dollars in damaged wood annually to oak stands, and adversely affect the form and vigor of oak regeneration. A moth and four species of beetles cause most of the damage; the carpenterworm moth, the oak timberworm, the red oak borer, the living-beech borer, and the white oak borer. The larvae of these insects chew holes in the wood ranging from...

Antioxidant enzymes GSR, SOD1, SOD2, and CAT gene variants and bone mineral density values in postmenopausal women: a genetic association analysis.

PubMed

Mlakar, Simona Jurkovic; Osredkar, Josko; Prezelj, Janez; Marc, Janja

2012-03-01

Oxidative stress participates in decreasing bone formation and stimulating bone resorption. Furthermore, antioxidant enzymes have been observed to have low protective activity in women with osteoporosis.The aim of the present study was to examine any association of selected gene polymorphisms of the glutathione S-reductase (GSR), superoxide dismutase (SOD1 and SOD2), and catalase (CAT) genes, alone or in combination, with the bone mineral density (BMD) values of femoral neck (fn), lumbar spine (ls), and total hip (th) in Slovenian postmenopausal women. The gene polymorphisms of CAT, GSR, SOD1, and SOD2 genes in 468 postmenopausal women were analyzed using restriction fragment length polymorphism and a fluorescent 5'-exonuclease genotyping method. BMD_fn, BMD_ls, and BMD_th were measured using dual-energy x-ray absorptiometry. Moreover, univariate statistic analysis and two-way analysis of variance for interaction testing were performed. A significant association of BMD_th values (P = 0.027) was found in genotype subgroups of 423-287G>A GSR polymorphism located in the third intron among postmenopausal women. Furthermore, women with at least one G allele showed significantly higher levels of BMD_fn (P = 0.044), BMD_th (P = 0.009), and BMD_ls (P = 0.043) than those that are AA homozygotes. Interestingly, the 423-287G>A_GSR*1154-393T>A_GSR combination was significantly associated with BMD_fn (P = 0.013) and BMD_th (P = 0.002) in postmenopausal women. The results of our study demonstrate for the first time that antioxidant enzyme GSR gene polymorphisms are significantly associated with BMD, suggesting that the A allele of 423-287G>A GSR polymorphism could contribute to decreased BMD values in postmenopausal women.

How to identify and manage oak wilt in Texas

Treesearch

D.N. Appel; R.S. Cameron; A.D. Wilson; J.D. Johnson

2008-01-01

Transporting unseasoned firewood from diseased red oaks is a potential means of spreading the oak wilt fungus. Oak wilt cannot be transmitted by burning infected firewood, but fungal mats may form on firewood in storage. Presently, no vectors have been proven to transmit the fungus from live oaks to other oak trees, but diseased wood fromany oak species should never be...

Regenerating oaks with the shelterwood system

Treesearch

Ivan L. Sander

1979-01-01

It is well known that a new reproduction stand that follows complete overstory removal will contain oaks in proportion to the numbers and size of advance oak reproduction present before the overstory was removed. Furthermore, the individual advance oaks must be relatively large with well-established root systems before they will compete successfully and be dominant in...

Accelerating the kiln drying of oak

Treesearch

William T. Simpson

1980-01-01

Reducing kiln-drying time for oak lumber can reduce energy requirements as well as reduce lumber inventories. In this work, l-inch northern red oak and white oak were kiln dried from green by a combination of individual accelerating techniques– presurfacing, presteaming, accelerated and smooth schedule, and high-temperature drying below 18 percent moisture content....

EXAFS analysis of a human Cu,Zn SOD isoform focused using non-denaturing gel electrophoresis

NASA Astrophysics Data System (ADS)

Chevreux, Sylviane; Solari, Pier Lorenzo; Roudeau, Stéphane; Deves, Guillaume; Alliot, Isabelle; Testemale, Denis; Hazemann, Jean Louis; Ortega, Richard

2009-11-01

Isoelectric point isoforms of a metalloprotein, copper-zinc superoxide dismutase (CuZnSOD), separated on electrophoresis gels were analyzed using X-ray Absorption Spectroscopy. Mutations of this protein are involved in familial cases of amyotrophic lateral sclerosis. The toxicity of mutants could be relied to defects in the metallation state. Our purpose is to establish analytical protocols to study metallation state of protein isoforms such as those from CuZnSOD. We previously highlighted differences in the copper oxidation state between CuZnSOD isoforms using XANES. Here, we present the first results for EXAFS analyses performed at Cu and Zn K-edge on the majoritary expressed isoform of human CuZnSOD separated on electrophoresis gels.

A semisynthetic strategy leads to alteration of the backbone amidate ligand in the NiSOD active site

DOE PAGES

Campeciño, Julius O.; Dudycz, Lech W.; Tumelty, David; ...

2015-07-01

Computational investigations have implicated the amidate ligand in nickel superoxide dismutase (NiSOD) in stabilizing Ni-centered redox catalysis and in preventing cysteine thiolate ligand oxidation. To test these predictions, we have used an experimental approach utilizing a semisynthetic scheme that employs native chemical ligation of a pentapeptide (HCDLP) to recombinant S. coelicolor NiSOD lacking these N-terminal residues, NΔ5-NiSOD. Wild-type enzyme produced in this manner exhibits the characteristic spectral properties of recombinant WT-NiSOD and is as catalytically active. The semisynthetic scheme was also employed to construct a variant where the amidate ligand was converted to a secondary amine, H1*-NiSOD, a novel strategymore » that retains a backbone N-donor atom. The H1*-NiSOD variant was found to have only ~1% of the catalytic activity of the recombinant wild-type enzyme, and had altered spectroscopic properties. X-ray absorption spectroscopy reveals a four-coordinate planar site with N 2S 2-donor ligands, consistent with electronic absorption spectroscopic results indicating that the Ni center in H1*-NiSOD is mostly reduced in the as-isolated sample, as opposed to 50:50 Ni(II)/Ni(III) mixture that is typical for the recombinant wild-type enzyme. The EPR spectrum of as-isolated H1*-NiSOD accounts for ~11% of the Ni in the sample and is similar to WT-NiSOD, but more axial, with g z < g x,y. 14N-hyperfine is observed on g z« less

Mammal caching of oak acorns in a red pine and a mixed oak stand

Treesearch

E.R. Thorn; W.M. Tzilkowski

1991-01-01

Small mammal caching of oak (Quercus spp.) acorns in adjacent red pine (Pinus resinosa) and mixed-oak stands was investigated at The Penn State Experimental Forest, Huntingdon Co., Pennsylvania. Gray squirrels (Sciurus carolinensis) and mice (Peromyscus spp.) were the most common acorn-caching...

Biological effects of CCS in the absence of SOD1 enzyme activation: implications for disease in a mouse model for ALS.

PubMed

Proescher, Jody B; Son, Marjatta; Elliott, Jeffrey L; Culotta, Valeria C

2008-06-15

The CCS copper chaperone is critical for maturation of Cu, Zn-superoxide dismutase (SOD1) through insertion of the copper co-factor and oxidization of an intra-subunit disulfide. The disulfide helps stabilize the SOD1 polypeptide, which can be particularly important in cases of amyotrophic lateral sclerosis (ALS) linked to misfolding of mutant SOD1. Surprisingly, however, over-expressed CCS was recently shown to greatly accelerate disease in a G93A SOD1 mouse model for ALS. Herein we show that disease in these G93A/CCS mice correlates with incomplete oxidation of the SOD1 disulfide. In the brain and spinal cord, CCS over-expression failed to enhance oxidation of the G93A SOD1 disulfide and if anything, effected some accumulation of disulfide-reduced SOD1. This effect was mirrored in culture with a C244,246S mutant of CCS that has the capacity to interact with SOD1 but can neither insert copper nor oxidize the disulfide. In spite of disulfide effects, there was no evidence for increased SOD1 aggregation. If anything, CCS over-expression prevented SOD1 misfolding in culture as monitored by detergent insolubility. This protection against SOD1 misfolding does not require SOD1 enzyme activation as the same effect was obtained with the C244,246S allele of CCS. In the G93A SOD1 mouse, CCS over-expression was likewise associated with a lack of obvious SOD1 misfolding marked by detergent insolubility. CCS over-expression accelerates SOD1-linked disease without the hallmarks of misfolding and aggregation seen in other mutant SOD1 models. These studies are the first to indicate biological effects of CCS in the absence of SOD1 enzymatic activation.

Association between activities of SOD, MDA and Na+-K+-ATPase in peripheral blood of patients with acute myocardial infarction and the complication of varying degrees of arrhythmia.

PubMed

Yin, Yu; Han, Wei; Cao, Ying

2018-04-24

To investigate the changes of ambulatory electrocardiography and peripheral blood SOD, MDA and Na+-K+-ATP enzymes in patients of acute myocardial infarction (AMI) complicated with arrhythmia. From January 2012 to March 2015, 135 cases AMI complicated with arrhythmia in our hospital were divided into 2 groups: 70 cases in the AMI uncomplicated with arrhythmia and 65 cases in the AMI complicated with arrhythmia. 62 cases volunteers accepted physical examination in our hospital in the same period were collected as the control group. 24 hour-electrocardiogram detected by ambulatory electrocardiogram (AECG), SOD and MDA in peripheral blood detected by diagnostic reagent kit and Na+-K+-ATP enzymes in peripheral blood detected by malachite green Kit Method phosphate determination method were collected. ROC curve was used to evaluate the prognostic value of SOD, MDA and Na+-K+-ATP enzymes in AMI patients. Compared with the control group, the patients had unusual ambulatory electrocardiography had increased (P <0.05), peripheral blood SOD and Na+-K+-ATP enzymes had decreased, peripheral blood MDA had increased in 2 AMI groups (P <0.05). Compared with AMI uncomplicated with arrhythmia group, the patients had unusual ambulatory electrocardiography had increased (P <0.05), peripheral blood SOD and Na+-K+-ATP enzymes had decreased, peripheral blood MDA had increased in AMI complicated with arrhythmia group (P <0.05). Among 135 cases AMI patients, 120 (88.9%) survived and 15 (11.1%) died, of whom 11 cases were AMI complicated with arrhythmia group, 4 cases were AMI uncomplicated with arrhythmia group. Compared with the AMI uncomplicated with arrhythmia group, the dead patients were more in the AMI complicated with arrhythmia group (c2 = 4.287, P = 0.038). Compared with the survival group, the SOD and Na+-K+-ATP enzymes were significantly lower (P <0.05) and MDA significantly higher (P <0.05) in the death group. The area under the ROC curve of SOD, MDA and Na+-K+-ATP enzymes

Coast live oak, Quercus agrifolia, susceptibility and response to goldspotted oak borer, Agrilus auroguttatus, injury in southern California

Treesearch

Tom W. Coleman; Nancy E. Grulke; Miles Daly; Cesar Godinez; Susan L. Schilling; Philip J. Riggan; Steven J. Seybold

2011-01-01

Oak mortality is often associated with a complex of decline factors. We describe the morphological and physiological responses of coast live oak, Quercus agrifolia Née, in California to an invasive insect, the goldspotted oak borer (GSOB), Agrilus auroguttatus Schaeffer (Coleoptera: Buprestidae), and evaluate drought as a...

Spontaneous abortion and functional polymorphism (Val16Ala) in the manganese SOD gene.

PubMed

Eskafi Sabet, E; Salehi, Z; Khodayari, S; Sabouhi Zarafshan, S; Zahiri, Z

2015-02-01

Spontaneous abortion is the most common complication of early pregnancy. Genetic factors have been hypothesised to play a role in spontaneous abortion. Since it is possible that the balance of oxidants and antioxidants can be affected by different genetic variants, gene polymorphisms have been proposed as a susceptibility factor that increases the chance of miscarriage. Manganese superoxide dismutase is an important antioxidant enzyme encoded by manganese superoxide dismutase (MnSOD) gene. The aim of this experiment was to assess whether Val16Ala polymorphism of MnSOD gene is associated with miscarriage in northern Iran. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used for genotyping. Statistical analyses were conducted using the χ(2)-test. The genetic distributions did not differ significantly between cases and controls, however slightly more Val/Val genotypes were found among the patients compared with control subjects (p = 0.059). No correlation was observed between susceptibility to abortion and MnSOD Val16Ala polymorphism. Larger population-based studies are needed for clarifying the relationship between abortion and MnSOD genotypes.

Working and Learning Among California Oaks

NASA Astrophysics Data System (ADS)

Tietje, B.; Gingg, B.; Zingo, J.; Huntsinger, L.

2009-04-01

With tremendous support from collaborators and enthusiastic volunteers, "Learning Among the Oaks" at the historic Santa Margarita Ranch has become a favorite outdoor learning experience for hundreds of Santa Margarita School students, along with their teachers and families. Oaks are at the center of this unique and cost effective public education program. From getting to know local oaks to exploring conservation issues within the context of a historic working cattle ranch, students take pride in expanding their awareness and knowledge of the local oak woodland community. Santa Margarita School families representing the varied demographics of the community come together on the trail. For many, the program provides a first opportunity to get to know those who make a living on the land and to understand that this land around their school is more than a pretty view. "Learning Among the Oaks" also addresses the need for quality, hands-on science activities and opportunities to connect children with the outdoor world. Using a thematic approach and correlating lessons with State Science Standards, we've engaged students in a full-spectrum of exciting outdoor learning adventures. As students progress through the grades, they find new challenges within the oak trail environment. We've succeeded in establishing an internship program that brings highly qualified, enthusiastic university students out to practice their science teaching skills while working with elementary school students. In the future, these university student interns may assist with the development of interpretive displays, after-school nature activities and monitoring projects. We've benefited from proximity to Cal Poly State University and its "learn-by-doing" philosophy. We've also succeeded in building a dedicated network of volunteers and collaborators, each with a special interest satisfied through participation in the oak trail program. While "Learning Among the Oaks" has focused on educating school

Establishment patterns of Oregon white oak and California black oak woodlands in northwestern California

Treesearch

Madelinn Schriver; Rosemary Sherriff

2015-01-01

Mixed-Oregon white oak (Quercus garryana) and California black oak (Q. kelloggii) woodlands are unique ecosystems that support high biodiversity in the Pacific Northwest, yet little is known about their current and historical stand establishment patterns in northwestern California. With concerns of local extirpation due to...

Mitochondrial dynamics and bioenergetic dysfunction is associated with synaptic alterations in mutant SOD1 motor neurons

PubMed Central

Magrané, Jordi; Sahawneh, Mary Anne; Przedborski, Serge; Estévez, Álvaro G.; Manfredi, Giovanni

2012-01-01

Mutations in Cu,Zn superoxide dismutase (SOD1) cause familial amyotrophic lateral sclerosis (FALS), a rapidly fatal motor neuron disease. Mutant SOD1 has pleiotropic toxic effects on motor neurons, among which mitochondrial dysfunction has been proposed as one of the contributing factors in motor neuron demise. Mitochondria are highly dynamic in neurons; they are constantly reshaped by fusion and move along neurites to localize at sites of high-energy utilization, such as synapses. The finding of abnormal mitochondria accumulation in neuromuscular junctions, where the SOD1-FALS degenerative process is though to initiate, suggests that impaired mitochondrial dynamics in motor neurons may be involved in pathogenesis. We addressed this hypothesis by live imaging microscopy of photo-switchable fluorescent mitoDendra in transgenic rat motor neurons expressing mutant or wild type human SOD1. We demonstrate that mutant SOD1 motor neurons have impaired mitochondrial fusion in axons and cell bodies. Mitochondria also display selective impairment of retrograde axonal transport, with reduced frequency and velocity of movements. Fusion and transport defects are associated with smaller mitochondrial size, decreased mitochondrial density, and defective mitochondrial membrane potential. Furthermore, mislocalization of mitochondria at synapses among motor neurons, in vitro, correlates with abnormal synaptic number, structure, and function. Dynamics abnormalities are specific to mutant SOD1 motor neuron mitochondria, since they are absent in wild type SOD1 motor neurons, they do not involve other organelles, and they are not found in cortical neurons. Taken together, these results suggest that impaired mitochondrial dynamics may contribute to the selective degeneration of motor neurons in SOD1-FALS. PMID:22219285

Transpiration of oak trees in the oak savannas of the Southwestern Borderlands region

Treesearch

Peter F. Ffolliott; Cody L. Stropki; Aaron T. Kauffman; Gerald J. Gottfried

2008-01-01

Transpiration of oak trees on the Cascabel watersheds in the savannas on the eastern slope of the Peloncillo Mountains in southwestern New Mexico has been estimated by the sap-flow method. Transpiration represents the largest loss of gross precipitation falling on a watershed in approximations of water budgets for the more densely stocked oak woodlands of the...

Single chain variable fragment antibodies block aggregation and toxicity induced by familial ALS-linked mutant forms of SOD1.

PubMed

Ghadge, Ghanashyam D; Pavlovic, John D; Koduvayur, Sujatha P; Kay, Brian K; Roos, Raymond P

2013-08-01

Approximately 10% of amyotrophic lateral sclerosis (ALS) cases are familial (known as FALS) with an autosomal dominant inheritance pattern, and ~25% of FALS cases are caused by mutations in Cu/Zn superoxide dismutase (SOD1). There is convincing evidence that mutant SOD1 (mtSOD1) kills motor neurons (MNs) because of a gain-of-function toxicity, most likely related to aggregation of mtSOD1. A number of recent reports have suggested that antibodies can be used to treat mtSOD1-induced FALS. To follow up on the use of antibodies as potential therapeutics, we generated single chain fragments of variable region antibodies (scFvs) against SOD1, and then expressed them as 'intrabodies' within a motor neuron cell line. In the present study, we describe isolation of human scFvs that interfere with mtSOD1 in vitro aggregation and toxicity. These scFvs may have therapeutic potential in sporadic ALS, as well as FALS, given that sporadic ALS may also involve abnormalities in the SOD1 protein or activity. Copyright © 2013 Elsevier Inc. All rights reserved.

Comparative study of antioxidant properties and total phenolic content of 30 plant extracts of industrial interest using DPPH, ABTS, FRAP, SOD, and ORAC assays.

PubMed

Dudonné, Stéphanie; Vitrac, Xavier; Coutière, Philippe; Woillez, Marion; Mérillon, Jean-Michel

2009-03-11

Aqueous extracts of 30 plants were investigated for their antioxidant properties using DPPH and ABTS radical scavenging capacity assay, oxygen radical absorbance capacity (ORAC) assay, superoxide dismutase (SOD) assay, and ferric reducing antioxidant potential (FRAP) assay. Total phenolic content was also determined by the Folin-Ciocalteu method. Antioxidant properties and total phenolic content differed significantly among selected plants. It was found that oak (Quercus robur), pine (Pinus maritima), and cinnamon (Cinnamomum zeylanicum) aqueous extracts possessed the highest antioxidant capacities in most of the methods used, and thus could be potential rich sources of natural antioxidants. These extracts presented the highest phenolic content (300-400 mg GAE/g). Mate (Ilex paraguariensis) and clove (Eugenia caryophyllus clovis) aqueous extracts also showed strong antioxidant properties and a high phenolic content (about 200 mg GAE/g). A significant relationship between antioxidant capacity and total phenolic content was found, indicating that phenolic compounds are the major contributors to the antioxidant properties of these plants.

HOW to Identify, Prevent, and Control Oak Wilt

Treesearch

Joseph O' Brien; Manfred Mielke; Dale Starkey; Jennifer Juzwik

2000-01-01

Oak wilt is an aggressive disease that affects many species of oak (Quercus spp.). It is one of the most serious tree diseases in the eastern United States, killing thousands of oaks each year in forests, woodlots, and home landscapes. Oak wilt was first identified in 1944. The fungal pathogen that causes the disease, Ceratocystis fagacearum, is thought by...

Postmitotic Expression of SOD1G93A Gene Affects the Identity of Myogenic Cells and Inhibits Myoblasts Differentiation

PubMed Central

Martini, Martina; Dobrowolny, Gabriella; Aucello, Michela; Musarò, Antonio

2015-01-01

To determine the role of mutant SOD1 gene (SOD1G93A) on muscle cell differentiation, we derived C2C12 muscle cell lines carrying a stably transfected SOD1G93A gene under the control of a myosin light chain (MLC) promoter-enhancer cassette. Expression of MLC/SOD1G93A in C2C12 cells resulted in dramatic inhibition of myoblast differentiation. Transfected SOD1G93A gene expression in postmitotic skeletal myocytes downregulated the expression of relevant markers of committed and differentiated myoblasts such as MyoD, Myogenin, MRF4, and the muscle specific miRNA expression. The inhibitory effects of SOD1G93A gene on myogenic program perturbed Akt/p70 and MAPK signaling pathways which promote differentiation cascade. Of note, the inhibition of the myogenic program, by transfected SOD1G93A gene expression, impinged also the identity of myogenic cells. Expression of MLC/SOD1G93A in C2C12 myogenic cells promoted a fibro-adipogenic progenitors (FAPs) phenotype, upregulating HDAC4 protein and preventing the myogenic commitment complex BAF60C-SWI/SNF. We thus identified potential molecular mediators of the inhibitory effects of SOD1G93A on myogenic program and disclosed potential signaling, activated by SOD1G93A, that affect the identity of the myogenic cell population. PMID:26491230

Postmitotic Expression of SOD1(G93A) Gene Affects the Identity of Myogenic Cells and Inhibits Myoblasts Differentiation.

PubMed

Martini, Martina; Dobrowolny, Gabriella; Aucello, Michela; Musarò, Antonio

2015-01-01

To determine the role of mutant SOD1 gene (SOD1(G93A)) on muscle cell differentiation, we derived C2C12 muscle cell lines carrying a stably transfected SOD1(G93A) gene under the control of a myosin light chain (MLC) promoter-enhancer cassette. Expression of MLC/SOD1(G93A) in C2C12 cells resulted in dramatic inhibition of myoblast differentiation. Transfected SOD1(G93A) gene expression in postmitotic skeletal myocytes downregulated the expression of relevant markers of committed and differentiated myoblasts such as MyoD, Myogenin, MRF4, and the muscle specific miRNA expression. The inhibitory effects of SOD1(G93A) gene on myogenic program perturbed Akt/p70 and MAPK signaling pathways which promote differentiation cascade. Of note, the inhibition of the myogenic program, by transfected SOD1(G93A) gene expression, impinged also the identity of myogenic cells. Expression of MLC/SOD1(G93A) in C2C12 myogenic cells promoted a fibro-adipogenic progenitors (FAPs) phenotype, upregulating HDAC4 protein and preventing the myogenic commitment complex BAF60C-SWI/SNF. We thus identified potential molecular mediators of the inhibitory effects of SOD1(G93A) on myogenic program and disclosed potential signaling, activated by SOD1(G93A), that affect the identity of the myogenic cell population.

Molecular and expression analysis of manganese superoxide dismutase (Mn-SOD) gene under temperature and starvation stress in rotifer Brachionus calyciflorus.

PubMed

Yang, Jianghua; Dong, Siming; Zhu, Huanxi; Jiang, Qichen; Yang, Jiaxin

2013-04-01

Superoxide dismutase (SOD) is an important antioxidant enzyme that protects organs from damage by reactive oxygen species. We cloned cDNA encoding SOD activated with manganese (Mn-SOD) from the rotifer Brachionus calyciflorus Pallas. The full-length cDNA of Mn-SOD was 1,016 bp and had a 669 bp open reading frame encoding 222 amino acids. The deduced amino acid sequence of B. calyciflorus Mn-SOD showed 89.1, 71.3, and 62.1 % similarity with the Mn-SOD of the marine rotifer Brachionus plicatilis, the nematode Caenorhabditis elegans, and the fruit fly Drosophila melanogaster, respectively. The phylogenetic tree constructed based on the amino acid sequences of Mn-SODs from B. calyciflorus and other organisms revealed that this rotifer is closely related to nematodes. Analysis of the mRNA expression of Mn-SOD under different conditions revealed that expression was enhanced 5.6-fold (p < 0.001) at 30 °C after 2 h, however, low temperature (15 °C) promoted Mn SOD temporarily (2.5-fold, p < 0.001) and then decreased to normal level (p > 0.05). Moderate starvation promoted Mn-SOD mRNA expression (p 12 < 0.01, p 36 < 0.05), which reached a maximum value (15.3 times higher than control, p 24 < 0.01) at 24 h. SOD and CAT activities also elevated at the 12 h-starved group. These results indicate that induction of Mn-SOD expression by stressors likely plays an important role in aging of B. calyciflorus.

Effect of the French Oak Wood Extract Robuvit on Markers of Oxidative Stress and Activity of Antioxidant Enzymes in Healthy Volunteers: A Pilot Study

PubMed Central

Orszaghova, Zuzana; Laubertova, Lucia; Sabaka, Peter; Rohdewald, Peter; Durackova, Zdenka; Muchova, Jana

2014-01-01

We examined in vitro antioxidant capacity of polyphenolic extract obtained from the wood of oak Quercus robur (QR), Robuvit, using TEAC (Trolox equivalent antioxidant capacity) method and the effect of its intake on markers of oxidative stress, activity of antioxidant enzymes, and total antioxidant capacity in plasma of 20 healthy volunteers. Markers of oxidative damage to proteins, DNA, and lipids and activities of Cu/Zn-superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were determined in the erythrocytes. We have found an in vitro antioxidant capacity of Robuvit of 6.37 micromole Trolox equivalent/mg of Robuvit. One month intake of Robuvit in daily dose of 300 mg has significantly decreased the serum level of advanced oxidation protein products (AOPP) and lipid peroxides (LP). Significantly increased activities of SOD and CAT as well as total antioxidant capacity of plasma after one month intake of Robuvit have been shown. In conclusion, we have demonstrated for the first time that the intake of Robuvit is associated with decrease of markers of oxidative stress and increase of activity of antioxidant enzymes and total antioxidant capacity of plasma in vivo. PMID:25254080

Response of chestnut oak and red oak to drought and fertilization: growth and physiology

Treesearch

M.D. Kleiner; M.D. Abrams; J.C. Schultz

1991-01-01

Chestnut oak (Quercus prinus L.) and red oak (Quercus rubra L.) seedlings were grown for two seasons under two nutrient regimes: fertilizer + (NPK) and fertilizer - (No NPK). Beginning two weeks after budbreak, water was withheld for 10 weeks during the second growing season. Leaf water potentials, gas exchange measurements and...

Interrelations of green oak leaf roller population and common oak: results of 30-year monitoring and mathematical modeling

Treesearch

V. V. Rubtsov; I. A. Utkina

2003-01-01

Long-term monitoring followed by mathematical modeling was used to describe the population dynamics of the green oak leaf roller Tortrix viridana L. over a period of 30 years and to study reactions of oak stands to different levels of defoliation. The mathematical model allows us to forecast the population dynamics of the green oak leaf roller and...

A meta-analysis of the fire-oak hypothesis: Does prescribed burning promote oak reproduction in eastern North America

Treesearch

Patrick H. Brose; Daniel C. Dey; Ross J. Phillips; Thomas A. Waldrop

2013-01-01

The fire-oak hypothesis asserts that the current lack of fire is a reason behind the widespread oak (Quercus spp.) regeneration difficulties of eastern North America, and use of prescribed burning can help solve this problem. We performed a meta-analysis on the data from 32 prescribed fire studies conducted in mixed-oak forests to test whether they...

The Use of Soil Scarification to Enhance Oak Regeneration in a Mixed-Oak Bottomland Forest of Southern Illinois

Treesearch

John M. Lhotka; James J. Zaczek

2002-01-01

The purpose of the study was to investigate whether soil scarification following seed fall can be used to increase the density of oak regeneration in a mixed-oak stand. The study area was a 4.5-hectare stand dominated by cherrybark oak (Quercus pagoda Eli.). The understory had a high percent cover of poison ivy (Toxicodendron radicans...

Unraveling ALS due to SOD1 mutation through the combination of brain and cervical cord MRI.

PubMed

Agosta, Federica; Spinelli, Edoardo Gioele; Marjanovic, Ivan V; Stevic, Zorica; Pagani, Elisabetta; Valsasina, Paola; Salak-Djokic, Biljana; Jankovic, Milena; Lavrnic, Dragana; Kostic, Vladimir S; Filippi, Massimo

2018-02-20

To explore structural and functional changes of the brain and cervical cord in patients with amyotrophic lateral sclerosis (ALS) due to mutation in the superoxide dismutase ( SOD1 ) gene compared with sporadic ALS. Twenty patients with SOD1 ALS, 11 with sporadic ALS, and 33 healthy controls underwent clinical evaluation and brain MRI. Cortical thickness analysis, diffusion tensor MRI of the corticospinal tracts (CST) and corpus callosum, and resting-state functional connectivity were performed. Patients with ALS also underwent cervical cord MRI to evaluate cord cross-sectional area and magnetization transfer ratio (MTR). Patients with SOD1 ALS showed longer disease duration and slower rate of functional decline relative to those with sporadic ALS. No cortical thickness abnormalities were found in patients with ALS compared with controls. Fractional anisotropy showed that sporadic ALS patients had significant CST damage relative to both healthy controls ( p = 0.001-0.02) and SOD1-related ALS ( p = 0.05), although the latter showed alterations that were intermediate between controls and sporadic ALS. Functional hyperconnectivity of the motor cortex in the sensorimotor network was observed in patients with sporadic ALS relative to controls. Conversely, patients with SOD1 ALS showed lower cord cross-sectional area along the whole cervical cord relative to those with sporadic ALS ( p < 0.001). No cord MTR differences were found between patient groups. Patients with SOD1 ALS showed cervical cord atrophy relative to those with sporadic ALS and a relative preservation of brain motor structural and functional networks. Neurodegeneration in SOD1 ALS is likely to occur primarily in the spinal cord. An objective and accurate estimate of spinal cord damage has potential in the future assessment of preventive SOD1 ALS therapies. © 2018 American Academy of Neurology.

Efficacy of Alamo for prophylactic and therapeutic treatment of oak wilt in red oaks, 2004

Treesearch

K. Ward; J. Juzwik; S. Bernick

2004-01-01

An experiment (prophylactic study) to determine the efficacy of Alamo in preventing spread of C. fagacearum through grafted roots of oak wilt-affected and of apparently healthy red oaks was initiated in eight locations in east-central and southeastern Minnesota in Jul 2002.

Auger planting of oak seedlings in northern Arkansas

Treesearch

Eric Heitzman; Adrian Grell

2003-01-01

Planting oak seedlings to regenerate upland oak forests is a promising but untested silvicultural practice in the Ozark Mountains of northern Arkansas. The stony (cherty) soils of the region make it difficult to dig deep planting holes using conventional hand planting tools. In 2001, we planted 1-0 northern red oak and white oak seedlings in 0.5 to 1 acre group...

The supply and demand situation for oak timber

Treesearch

Kenneth L. Quigley

1971-01-01

Twenty oak species in the eastern United States account for one-third of the hardwood sawtimber volume and almost 10 percent of both hardwood and softwood growing-stock volume. The oak-hickory and oak-pine forest types occupy about 38 percent of the forest land in the eastern United States. Oak timber volume is increasing. Annual growth exceeds annual removals by about...

Determining the Effect of Catechins on SOD1 Conformation and Aggregation by Ion Mobility Mass Spectrometry Combined with Optical Spectroscopy

NASA Astrophysics Data System (ADS)

Zhao, Bing; Zhuang, Xiaoyu; Pi, Zifeng; Liu, Shu; Liu, Zhiqiang; Song, Fengrui

2018-02-01

The aggregation of Cu,Zn-superoxide dismutase (SOD1) plays an important role in the etiology of amyotrophic lateral sclerosis (ALS). For the disruption of ALS progression, discovering new drugs or compounds that can prevent SOD1 aggregation is important. In this study, ESI-MS was used to investigate the interaction of catechins and SOD1. The noncovalent complex of catechins that interact with SOD1 was found and retained in the gas phase under native ESI-MS condition. The conformation changes of SOD1 after binding with catechins were also explored via traveling wave ion mobility (IM) spectrometry. Epigallocatechin gallate (EGCG) can stabilize SOD1 conformation against unfolding in three catechins. To further evaluate the efficacy of EGCG, we monitored the fluorescence changes of dimer E2,E2,-SOD1(apo-SOD1, E:empty) with and without ligands under denaturation conditions, and found that EGCG can inhibit apo-SOD1 aggregation. In addition, the circular dichroism spectra of the samples showed that EGCG can decrease the β-sheet content of SOD1, which can produce aggregates. These results indicated that orthogonal separation dimension in the gas-phase IM coupled with ESI-MS (ESI-IM-MS) can potentially provide insight into the interaction between SOD1 and small molecules. The advantage is that it dramatically decreases the analysis time. Meantime, optical spectroscopy techniques can be used to confirm ESI-IM-MS results. [Figure not available: see fulltext.

Relative susceptibility of oaks to seven species of Phytophthora isolated from oak forest soils

Treesearch

Y. Balci; S. Balci; W.L. MacDonald; K.W. Gottschalk

2008-01-01

Isolates of Phytophthora cambivora, P. cinnamomi, P. citricola, P. europaea, P. quercetorum and two unidentified species were tested for their pathogenicity to eastern US oak species by root and stem inoculations. Experiments were conducted during two different periods and included 1-, 2- and 20- year-old oaks grown under greenhouse and field...

Comprehensive integrated planning: A process for the Oak Ridge Reservation, Oak Ridge, Tennessee

DOE Office of Scientific and Technical Information (OSTI.GOV)

NONE

1998-05-01

The Oak Ridge Comprehensive Integrated Plan is intended to assist the US Department of Energy (DOE) and contractor personnel in implementing a comprehensive integrated planning process consistent with DOE Order 430.1, Life Cycle Asset Management and Oak Ridge Operations Order 430. DOE contractors are charged with developing and producing the Comprehensive Integrated Plan, which serves as a summary document, providing information from other planning efforts regarding vision statements, missions, contextual conditions, resources and facilities, decision processes, and stakeholder involvement. The Comprehensive Integrated Plan is a planning reference that identifies primary issues regarding major changes in land and facility use andmore » serves all programs and functions on-site as well as the Oak Ridge Operations Office and DOE Headquarters. The Oak Ridge Reservation is a valuable national resource and is managed on the basis of the principles of ecosystem management and sustainable development and how mission, economic, ecological, social, and cultural factors are used to guide land- and facility-use decisions. The long-term goals of the comprehensive integrated planning process, in priority order, are to support DOE critical missions and to stimulate the economy while maintaining a quality environment.« less

Intestinal cell targeting of a stable recombinant Cu-Zn SOD from Cucumis melo fused to a gliadin peptide.

PubMed

Intes, Laurent; Bahut, Muriel; Nicole, Pascal; Couvineau, Alain; Guette, Catherine; Calenda, Alphonse

2012-05-31

The mRNA encoding full length chloroplastic Cu-Zn SOD (superoxide dismutase) of Cucumis melo (Cantaloupe melon) was cloned. This sequence was then used to generate a mature recombinant SOD by deleting the first 64 codons expected to encode a chloroplastic peptide signal. A second hybrid SOD was created by inserting ten codons to encode a gliadin peptide at the N-terminal end of the mature SOD. Taking account of codon bias, both recombinant proteins were successfully expressed and produced in Escherichia coli. Both recombinant SODs display an enzymatic activity of ~5000U mg(-1) and were shown to be stable for at least 4h at 37°C in biological fluids mimicking the conditions of intestinal transit. These recombinant proteins were capable in vitro, albeit at different levels, of reducing ROS-induced-apoptosis of human epithelial cells. They also stimulated production and release in a time-dependent manner of an autologous SOD activity from cells located into jejunum biopsies. Nevertheless, the fused gliadin peptide enable the recombinant Cu-Zn SOD to maintain a sufficiently sustained interaction with the intestinal cells membrane in vivo rather than being eliminated with the flow. According to these observations, the new hybrid Cu-Zn SOD should show promise in applications for managing inflammatory bowel diseases. Copyright © 2012 Elsevier B.V. All rights reserved.

Iowa's oldest oaks. [Quercus alba

DOE Office of Scientific and Technical Information (OSTI.GOV)

Duvick, D.N.; Blasing, T.J.

1983-01-01

Tree-ring analysis revealed 33 living white oaks (Quercus alba) in Iowa that began growing before 1700. Core of wood 4 mm in diameter, each extracted from a radius of a tree trunk were analyzed. The oldest white oak, found in northeastern Warren County, began growing about 1570 and is thus over 410 years old. A chinkapin oak (Quercus muehlenbergii) was also found which was more than 300 years old. Ring widths from the white oaks are well correlated with total precipitation for the twelve months preceding completion of ring formation in July. Reconstructions of annual (August-July) precipitation for 1680-1979, basedmore » on the tree rings, indicate that the driest annual period in Iowa was August 1799-July 1800, and that the driest decade began about 1816. Climatic information of this kind, pre-dating written weather records, can be used to augment those records and provide a longer baseline of information for use by climatologists and hydrologic planners.« less

Oak Decline and Red Oak Borer in the Interior Highlands of Arkansas an Missouri: Natural Phenomena, Severe Occurrences

Treesearch

Dale A. Starkey; Forrest Oliveria; Alexander Mangini; Manfred Mielke

2004-01-01

Oak decline is a complex disease resulting in dieback and mortality of oaks. A number of factors are involved and can be classified as predisposing, inciting, or contributing, according to their roles. Decline events have been noted repeatedly during the past century in the eastern U.S. A severe episode of oak decline is occurring in the Interior Highlands region of...

Cytoplasmic Copper Detoxification in Salmonella Can Contribute to SodC Metalation but Is Dispensable during Systemic Infection

PubMed Central

Fenlon, Luke A.

2017-01-01

ABSTRACT Salmonella enterica serovar Typhimurium is a leading cause of foodborne disease worldwide. Severe infections result from the ability of S. Typhimurium to survive within host immune cells, despite being exposed to various host antimicrobial factors. SodCI, a copper-zinc-cofactored superoxide dismutase, is required to defend against phagocytic superoxide. SodCII, an additional periplasmic superoxide dismutase, although produced during infection, does not function in the host. Previous studies suggested that CueP, a periplasmic copper binding protein, facilitates acquisition of copper by SodCII. CopA and GolT, both inner membrane ATPases that pump copper from the cytoplasm to the periplasm, are a source of copper for CueP. Using in vitro SOD assays, we found that SodCI can also utilize CueP to acquire copper. However, both SodCI and SodCII have a significant fraction of activity independent of CueP and cytoplasmic copper export. We utilized a series of mouse competition assays to address the in vivo role of CueP-mediated SodC activation. A copA golT cueP triple mutant was equally as competitive as the wild type, suggesting that sufficient SodCI is active to defend against phagocytic superoxide independent of CueP and cytoplasmic copper export. We also confirmed that a strain containing a modified SodCII, which is capable of complementing a sodCI deletion, was fully virulent in a copA golT cueP background competed against the wild type. These competitions also address the potential impact of cytoplasmic copper toxicity within the phagosome. Our data suggest that Salmonella does not encounter inhibitory concentrations of copper during systemic infection. IMPORTANCE Salmonella is a leading cause of gastrointestinal disease worldwide. In severe cases, Salmonella can cause life-threatening systemic infections, particularly in very young children, the elderly, or people who are immunocompromised. To cause disease, Salmonella must survive the hostile environment

Cytoplasmic Copper Detoxification in Salmonella Can Contribute to SodC Metalation but Is Dispensable during Systemic Infection.

PubMed

Fenlon, Luke A; Slauch, James M

2017-12-15

Salmonella enterica serovar Typhimurium is a leading cause of foodborne disease worldwide. Severe infections result from the ability of S Typhimurium to survive within host immune cells, despite being exposed to various host antimicrobial factors. SodCI, a copper-zinc-cofactored superoxide dismutase, is required to defend against phagocytic superoxide. SodCII, an additional periplasmic superoxide dismutase, although produced during infection, does not function in the host. Previous studies suggested that CueP, a periplasmic copper binding protein, facilitates acquisition of copper by SodCII. CopA and GolT, both inner membrane ATPases that pump copper from the cytoplasm to the periplasm, are a source of copper for CueP. Using in vitro SOD assays, we found that SodCI can also utilize CueP to acquire copper. However, both SodCI and SodCII have a significant fraction of activity independent of CueP and cytoplasmic copper export. We utilized a series of mouse competition assays to address the in vivo role of CueP-mediated SodC activation. A copA golT cueP triple mutant was equally as competitive as the wild type, suggesting that sufficient SodCI is active to defend against phagocytic superoxide independent of CueP and cytoplasmic copper export. We also confirmed that a strain containing a modified SodCII, which is capable of complementing a sodCI deletion, was fully virulent in a copA golT cueP background competed against the wild type. These competitions also address the potential impact of cytoplasmic copper toxicity within the phagosome. Our data suggest that Salmonella does not encounter inhibitory concentrations of copper during systemic infection. IMPORTANCE Salmonella is a leading cause of gastrointestinal disease worldwide. In severe cases, Salmonella can cause life-threatening systemic infections, particularly in very young children, the elderly, or people who are immunocompromised. To cause disease, Salmonella must survive the hostile environment inside host

Comparison of oak and sugar maple distribution and regeneration in central Illinois upland oak forests

Treesearch

Peter J. Frey; Scott J. Meiners

2014-01-01

Changes in disturbance frequencies, habitat fragmentation, and other biotic pressures are allowing sugar maple (Acer saccharum) to displace oak (Quercus spp.) in the upland forest understory. The displacement of oaks by sugar maples represents a major management concern throughout the region. We collected seedling microhabitat data...

An ecologically based approach to oak silviculture: a synthesis of 50 years of oak ecosystem research in North America

Treesearch

Daniel C. Dey; Alejandro A. Royo; Patrick H. Brose; Todd F. Hutchinson; Martin A. Spetich; Scott H. Stoleson

2010-01-01

Oak (Quercus L.) is an abundant and widely distributed genus in eastern North America. A history of periodic fire, grazing, canopy disturbance and timber harvesting has favored oak's dominance. But, changes in this regime toward much less fire or complete fire suppression, and selective cutting are causing the successional replacement of oak....

Fire in upper Midwestern oak forest ecosystems: an oak forest restoration and management handbook

Treesearch

Lee E. Frelich; Peter B. Reich; David W. Peterson

2015-01-01

We reviewed the literature to synthesize what is known about the use of fire to maintain and restore oak forests, woodlands, and savannas of the upper Midwestern United States, with emphasis on Minnesota, Wisconsin, and Michigan. Included are (1) known physical and ecological effects of fire on oaks from acorn through seedling, established sapling, and mature stages of...

Proceedings of the seventh California oak symposium: managing oak woodlands in a dynamic world

Treesearch

Richard B. Standiford; Kathryn L. Purcell

2015-01-01

Beginning in 1979, there have been a series of symposia held every 5 to 7 years addressing the state of our knowledge about science, policy and management factors affecting California's oak resource. This program represents the seventh symposium in the series. California's oak woodlands cover 10 percent of the state, and in addition, are a key ecological...

Oak Regeneration Using the Two-Age System

Treesearch

Jeffrey W. Stringer

2002-01-01

The two studies presented in this paper were completed in southeastern Kentucky and were designed to evaluate acorn production and development of advanced white oak reproduction from fully released white oak (Quercus alba) trees typical of reserve trees in the two age system. Twelve 2 acre 60- to 90-year-old white oak dominated stands were...

Response of Overtopped White Oak to Release

Treesearch

Charles E. McGee

1981-01-01

Pole sized white oaks increase in volume growth following release from overtopping trees, but the response varies by size, age and appearance of the oaks. Significant increases in epicormic sprouting, height loss by some released trees, and highly variable stem volume growth make overtopped white oak a very questionable source of future crop trees. If overtopped trees...

Oaks belowground: mycorrhizas, truffles, and small mammals

Treesearch

Jonathan Frank; Seth Barry; Joseph Madden; Darlene Southworth

2008-01-01

Oaks depend on hidden diversity belowground. Oregon white oaks (Quercus garryana) form ectomycorrhizas with more than 40 species of fungi at a 25-ha site. Several of the most common oak mycorrhizal fungi form hypogeous fruiting bodies or truffles in the upper layer of mineral soil. We collected 18 species of truffles associated with Oregon white...

Site and canopy characteristics associated with oak advance reproduction in mature oak-hickory forests in the ridge and valley province in Tennessee

Treesearch

Leslie S. Chadwell; David S. Buckley

2003-01-01

To investigate hypotheses regarding effects of competitors and site quality on oak regeneration, we documented site factors and oak seedling composition, size, and abundance in the Ridge and Valley Province of Tennessee. Small oak seedlings were most abundant on productive soils and mesic landform positions, whereas large oak seedlings were most abundant on less...

Oak decline

Treesearch

Kenneth J., Jr. Kessler; David R. Houston

1989-01-01

Oak declines are complex plant diseases that result when trees are first stressed by environmental factors and/or living organisms and are then invaded and sometimes killed by opportunistic secondary organisms.

Oak Regeneration - What We Know

Treesearch

Harvey E. Kennedy

1989-01-01

Growth and development of saplings of four-oak (Quercus spp.) species planted at five spacings in a minor stream bottom in southeast Arkansas showed significant differences among species and spacings. Spacing affected all tree size and biomass variables except survival. Yater oak (Q. nigra L.) developed most rapidly; swamp chestnut...

Monitoring oak-hickory forest change during an unprecedented red oak borer outbreak in the Ozark Mountains: 1990 to 2006

Treesearch

Joshua S. Jones; Jason A. Tullis; Laurel J. Haavik; James M. Guldin; Fred M. Stephen

2014-01-01

Upland oak-hickory forests in Arkansas, Missouri, and Oklahoma experienced oak decline in the late 1990s and early 2000s during an unprecedented outbreak of a native beetle, the red oak borer (ROB), Enaphalodes rufulus (Haldeman). Although remote sensing supports frequent monitoring of continuously changing forests, comparable in situ observations are critical for...

Clemson Researchers Find Prescribed Fire Regenerates Oak Forests

Treesearch

David van Lear; Patrick Brose

1999-01-01

Fire is being prescribed by Clemson University forestry researchers to regenerate oak forests. Regenerating oaks following timber harvests is a major challenge because faster growing yellow polar and red maple trees crowd out hte more valuable oak seedlings.

Esculetin Protects Human Retinal Pigment Epithelial Cells from Lipopolysaccharide-induced Inflammation and Cell Death.

PubMed

Ozal, S Altan; Turkekul, Kader; Gurlu, Vuslat; Guclu, Hande; Erdogan, Suat

2018-05-26

Age-related macular degeneration (AMD) is the most common cause of visual loss. The dry AMD is characterized by retinal pigment epithelium (RPE) death and changes in AMD lead to severe loss of vision. Coumarin-derived esculetin has a number of therapeutic and pharmacological effects such as anti-inflammatory and antioxidant with various mechanisms. The purpose of this study was to investigate the effects of esculetin treatment on lipopolysaccharide (LPS)-induced inflammation, oxidative stress, and cell survival. Human RPE cells (ARPE-19) were incubated for 24-72 h with 5 μg/ml LPS to induce inflammation and oxidative stress. Esculetin (5 μM) was used to protect the cells from LPS-induced damage. The cell viability was evaluated by quantitative 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide test. Interleukin 6 (IL-6), IL-12, and vascular endothelial growth factor (VEGF) levels were determined by enzyme-linked immunosorbent assay (ELISA). IL-1β, tumor necrosis factor receptor (TNFR), TNF-related apoptosis-inducing ligand (TRAIL), catalase, glutathione peroxidase (GPx), superoxide dismutase 1 (CuZnSOD) and SOD2 (MnSOD) mRNA expressions were analyzed by RT-quantitative polymerase chain reaction. Apoptosis was monitored by cell-based cytometer. NF-kappa B (NF-κB) p65/RelA levels were determined by ELISA, and NF-κB protein expression and extracellular signal-regulated kinase (ERK1/2) phosphorylation were evaluated by Western blot analysis. Esculetin treatment significantly suppressed LPS-induced cell death mediated by apoptosis and necrosis in a concentration-dependent manner. While LPS caused significant inflammation with cytokine increase in cells, esculetin reduced the expression of LPS-induced cytokines, VEGF, TNFR, and TRAIL. Furthermore, exposure to LPS increased the expression of GPx and mitochondrial MnSOD, leading to oxidative stress in the cells. Esculetin treatment attenuated phosphorylation of ERK1/2 and NF-κB expression mediated by LPS

Reactive oxygen species on bone mineral density and mechanics in Cu,Zn superoxide dismutase (Sod1) knockout mice

DOE Office of Scientific and Technical Information (OSTI.GOV)

Smietana, Michael J.; Arruda, Ellen M.; Mechanical Engineering, University of Michigan, 2250 GG Brown, 2350 Hayward, Ann Arbor, MI 48109

Research highlights: {yields} Reactive oxygen species (ROS) are considered to be a factor in the onset of a number of age-associated conditions, including loss of BMD. {yields} Cu,Zn-superoxide dismutase (Sod1) deficient mice have increased ROS, reduced bone mineral density, decreased bending stiffness, and decreased strength compared to WT controls. {yields} Increased ROS caused by the deficiency of Sod1, may be responsible for the changes in BMD and bone mechanics and therefore represent an appropriate model for studying mechanisms of age-associated bone loss. -- Abstract: Reactive oxygen species (ROS) play a role in a number of degenerative conditions including osteoporosis. Micemore » deficient in Cu,Zn-superoxide dismutase (Sod1) (Sod1{sup -/-} mice) have elevated oxidative stress and decreased muscle mass and strength compared to wild-type mice (WT) and appear to have an accelerated muscular aging phenotype. Thus, Sod1{sup -/-} mice may be a good model for evaluating the effects of free radical generation on diseases associated with aging. In this experiment, we tested the hypothesis that the structural integrity of bone as measured by bending stiffness (EI; N/mm{sup 2}) and strength (MPa) is diminished in Sod1{sup -/-} compared to WT mice. Femurs were obtained from male and female WT and Sod1{sup -/-} mice at 8 months of age and three-point bending tests were used to determine bending stiffness and strength. Bones were also analyzed for bone mineral density (BMD; mg/cc) using micro-computed tomography. Femurs were approximately equal in length across all groups, and there were no significant differences in BMD or EI with respect to gender in either genotype. Although male and female mice demonstrated similar properties within each genotype, Sod1{sup -/-} mice exhibited lower BMD and EI of femurs from both males and females compared with gender matched WT mice. Strength of femurs was also lower in Sod1{sup -/-} mice compared to WT as well as between genders

Seeding and planting upland oaks

Treesearch

T. E. Russell

1971-01-01

Upland oaks can be established by seeding or planting, but additional experience is needed before these methods become economical alternatives to natural regeneration. Recently forested sites are generally more favorable than abandoned fields. Lack of repellents to protect acorns from animals severely limits direct seeding, but oaks can be planted readily by...

Manufacture of industrial products from oak

Treesearch

Hugh W. Reynolds

1971-01-01

The three largest and fastest growing markets for oak are railroad crossties, reusable pallets, and truck and container flooring. Manufacturers of oak lumber are advised to keep these products in mind when planning their production.

Soil-site relationships of the upland oaks

Treesearch

Willard H. Carmean

1971-01-01

Site quality for upland oaks can be estimated directly by using site-index curves, or indirect estimations can be made by using soil-site prediction methods. Presently available harmonized site-index curves may not be suitable for all upland oak species, or may not be suitable throughout their range. New stem-analysis data show that different species of oak have...

Gypsy moth impacts on oak acorn production

Treesearch

Kurt W. Gottschalk