Pseudomonas syringae effector AvrPto blocks innate immunity by targeting receptor kinases

被引:365
|
作者
Xiang, Tingting [1 ,2 ]
Zong, Na [2 ]
Zou, Yan [2 ,3 ]
Wu, Yong [2 ]
Zhang, Jie [2 ]
Xing, Weiman [2 ]
Li, Yan [2 ]
Tang, Xiaoyan [4 ]
Zhu, Lihuang [3 ]
Chai, Jijie [2 ]
Zhou, Jian-Min [2 ]
机构
[1] China Agr Univ, State Key Lab Plant Physiol & Biochem, Coll Biol Sci, Beijing 100094, Peoples R China
[2] Natl Inst Biol Sci, Beijing 102206, Peoples R China
[3] Chinese Acad Sci, Inst Genet, Beijing 100864, Peoples R China
[4] Kansas State Univ, Dept Plant Pathol, Manhattan, KS 66506 USA
关键词
D O I
10.1016/j.cub.2007.12.020
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
Plants use receptor kinases, such as FLS2 and EFR, to perceive bacterial pathogens and initiate innate immunity. This immunity is often suppressed by bacterial effectors, allowing pathogen propagation. To counteract, plants have evolved disease resistance genes that detect the bacterial effectors and reinstate resistance. The Pseudomonas syringae effector AvrPto promotes infection in susceptible plants but triggers resistance in plants carrying the protein kinase Pto and the associated resistance protein Prf. Here we show that AvrPto binds receptor kinases, including Arabidopsis FLS2 and EFR and tomato LeFLS2, to block plant immune responses in the plant cell. The ability to target receptor kinases is required for the virulence function of AvrPto in plants. The FLS2-AvrPto interaction and Pto-AvrPto interaction appear to share similar sequence requirements, and Pto competes with FLS2 for AvrPto binding. The results suggest that the mechanism by which AvrPto recognizes virulence targets is linked to the evolution of Pto, which, in association with Prf, recognizes the bacterium and triggers strong resistance.
引用
收藏
页码:74 / 80
页数:7
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