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dc.contributor.author TeKippe, M
dc.contributor.author Aballay, A
dc.coverage.spatial United States
dc.date.accessioned 2011-06-21T17:31:33Z
dc.date.issued 2010-07-26
dc.identifier http://www.ncbi.nlm.nih.gov/pubmed/20668681
dc.identifier.citation PLoS One, 2010, 5 (7), pp. e11777 - ?
dc.identifier.uri http://hdl.handle.net/10161/4557
dc.description.abstract Reproduction extracts a cost in resources that organisms are then unable to utilize to deal with a multitude of environmental stressors. In the nematode C. elegans, development of the germline shortens the lifespan of the animal and increases its susceptibility to microbial pathogens. Prior studies have demonstrated germline-deficient nematodes to have increased resistance to gram negative bacteria. We show that germline-deficient strains display increased resistance across a broad range of pathogens including gram positive and gram negative bacteria, and the fungal pathogen Cryptococcus neoformans. Furthermore, we show that the FOXO transcription factor DAF-16, which regulates longevity and immunity in C. elegans, appears to be crucial for maintaining longevity in both wild-type and germline-deficient backgrounds. Our studies indicate that germline-deficient mutants glp-1 and glp-4 respond to pathogen infection using common and different mechanisms that involve the activation of DAF-16.
dc.format.extent e11777 - ?
dc.language eng
dc.language.iso en_US en_US
dc.relation.ispartof PLoS One
dc.relation.isversionof 10.1371/journal.pone.0011777
dc.subject Animals
dc.subject Animals, Genetically Modified
dc.subject Bacterial Physiological Phenomena
dc.subject Caenorhabditis elegans
dc.subject Caenorhabditis elegans Proteins
dc.subject Cryptococcus neoformans
dc.subject Forkhead Transcription Factors
dc.subject Gram-Negative Bacteria
dc.subject Gram-Positive Bacteria
dc.subject Immunity
dc.subject Longevity
dc.subject RNA Interference
dc.subject Transcription Factors
dc.title C. elegans germline-deficient mutants respond to pathogen infection using shared and distinct mechanisms.
dc.title.alternative en_US
dc.type Journal Article
dc.description.version Version of Record en_US
duke.date.pubdate 2010-7-26 en_US
duke.description.endpage e11777 en_US
duke.description.issue 7 en_US
duke.description.startpage e11777 en_US
duke.description.volume 5 en_US
dc.relation.journal Plos One en_US
pubs.author-url http://www.ncbi.nlm.nih.gov/pubmed/20668681
pubs.issue 7
pubs.organisational-group /Duke
pubs.organisational-group /Duke/Institutes and Provost's Academic Units
pubs.organisational-group /Duke/Institutes and Provost's Academic Units/University Institutes and Centers
pubs.organisational-group /Duke/Institutes and Provost's Academic Units/University Institutes and Centers/Duke Institute for Brain Sciences
pubs.organisational-group /Duke/School of Medicine
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments/Molecular Genetics and Microbiology
pubs.publication-status Published online
pubs.volume 5
dc.identifier.eissn 1932-6203

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