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dc.contributor.authorChibucos, Marcus Cen_US
dc.contributor.authorCollmer, Candace Wen_US
dc.contributor.authorTorto-Alalibo, Trudyen_US
dc.contributor.authorGwinn-Giglio, Michelleen_US
dc.contributor.authorLindeberg, Magdalenen_US
dc.contributor.authorLi, Donghuien_US
dc.contributor.authorTyler, Brett M.en_US
dc.date.accessioned2012-08-24T11:46:54Z
dc.date.available2012-08-24T11:46:54Z
dc.date.issued2009-02-19en_US
dc.identifier.citationBMC Microbiology. 2009 Feb 19;9(Suppl 1):S5en_US
dc.identifier.urihttp://hdl.handle.net/10919/18871
dc.description.abstractManipulation of programmed cell death (PCD) is central to many host microbe interactions. Both plant and animal cells use PCD as a powerful weapon against biotrophic pathogens, including viruses, which draw their nutrition from living tissue. Thus, diverse biotrophic pathogens have evolved many mechanisms to suppress programmed cell death, and mutualistic and commensal microbes may employ similar mechanisms. Necrotrophic pathogens derive their nutrition from dead tissue, and many produce toxins specifically to trigger programmed cell death in their hosts. Hemibiotrophic pathogens manipulate PCD in a most exquisite way, suppressing PCD during the biotrophic phase and stimulating it during the necrotrophic phase. This mini-review will summarize the mechanisms that have evolved in diverse microbes and hosts for controlling PCD and the Gene Ontology terms developed by the Plant-Associated Microbe Gene Ontology (PAMGO) Consortium for describing those mechanisms.en_US
dc.format.mimetypeapplication/pdfen_US
dc.language.isoen_USen_US
dc.rightsAttribution 4.0 United States*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.titleProgrammed cell death in host-symbiont associations, viewed through the Gene Ontologyen_US
dc.typeJournal articleen_US
dc.date.updated2012-08-24T11:46:54Z
dc.description.versionPeer Revieweden_US
dc.language.rfc3066enen_US
dc.rights.holderMarcus C Chibucos et al.; licensee BioMed Central Ltd.en_US
dc.identifier.doihttp://dx.doi.org/10.1186/1471-2180-9-S1-S5en_US
dc.type.dcmitypeTexten_US


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Attribution 4.0 United States
License: Attribution 4.0 United States