RIN4 interacts with Pseudomonas syringae type III effector molecules and is required for RPM1-mediated resistance in Arabidopsis

被引:913
作者
Mackey, D
Holt, BF
Wiig, A
Dangl, JL
机构
[1] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA
[2] Univ N Carolina, Dept Biol, Chapel Hill, NC 27599 USA
[3] Univ N Carolina, Curriculum Genet, Chapel Hill, NC 27599 USA
基金
美国国家科学基金会;
关键词
D O I
10.1016/S0092-8674(02)00661-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In Arabidopsis, RPM1 confers resistance against Pseudomonas syringae expressing either of two sequence unrelated type III effectors, AvrRpm1 or AvrB. An RPM1-interacting protein (RIN4) coimmunoprecipitates from plant cell extracts with AvrB, AvrRpm1, or RPM1. Reduction of RIN4 protein levels inhibits both the hypersensitive response and the restriction of pathogen growth controlled by RPM1. RIN4 reduction causes diminution of RPM1. RIN4 reduction results in heightened resistance to virulent Peronospora parasitica and P. syringae, and ectopic defense gene expression. Thus, RIN4 positively regulates RPM1-mediated resistance yet is, formally, a negative regulator of basal defense responses. AvrRpm1 and AvrB induce RIN4 phosphorylation. This may enhance RIN4 activity as a negative regulator of plant defense, facilitating pathogen growth. RPM1 may "guard" against pathogens that use AvrRpm1 and AvrB to manipulate RIN4 activity.
引用
收藏
页码:743 / 754
页数:12
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