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pubmed-article:15935761pubmed:dateCreated2005-6-6lld:pubmed
pubmed-article:15935761pubmed:abstractTextPlant cells have two defense systems that detect bacterial pathogens. One is a basal defense system that recognizes complex pathogen-associated molecular patterns (PAMPs). A second system uses disease-resistance (R) proteins to recognize type lll effector proteins that are delivered into the plant cell by the pathogen's type III secretion system. Here we show that these two pathways are linked. We find that two Pseudomonas syringae type III effectors, AvrRpt2 and AvrRpm1, inhibit PAMP-induced signaling and thus compromise the host's basal defense system. RIN4 is an Arabidopsis protein targeted by AvrRpt2 and AvrRpm1 for degradation and phosphorylation, respectively. We find that RIN4 is itself a regulator of PAMP signaling. The R proteins, RPS2 and RPM1, sense type III effector-induced perturbations of RIN4. Thus, R proteins guard the plant against type III effectors that inhibit PAMP signaling and provide a mechanistic link between the two plant defense systems.lld:pubmed
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pubmed-article:15935761pubmed:pagination749-59lld:pubmed
pubmed-article:15935761pubmed:dateRevised2009-11-19lld:pubmed
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pubmed-article:15935761pubmed:articleTitleTwo Pseudomonas syringae type III effectors inhibit RIN4-regulated basal defense in Arabidopsis.lld:pubmed
pubmed-article:15935761pubmed:affiliationDepartment of Plant Cellular and Molecular Biology, Program in Molecular Cellular and Developmental Biology, The Ohio State University, Columbus, Ohio 43210, USA.lld:pubmed
pubmed-article:15935761pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:15935761pubmed:publicationTypeResearch Support, U.S. Gov't, Non-P.H.S.lld:pubmed
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