TY - JOUR
T1 - Activation-Dependent Destruction of a Co-receptor by a Pseudomonas syringae Effector Dampens Plant Immunity
AU - Li, Lei
AU - Kim, Panya
AU - Yu, Liping
AU - Cai, Gaihong
AU - Chen, She
AU - Alfano, James R.
AU - Zhou, Jian Min
N1 - Funding Information:
We thank Dr. Cyril Zipfel for sharing bak1–5/bkk1 seeds. This work was funded by Chinese Natural Science Foundation (31320103909), the Chinese Ministry of Science and Technology grant 2015CB910200, the Strategic Priority Research Program of the Chinese Academy of Sciences (grant number XDB11020200), the Chinese Academy of Sciences international cooperation key project grant GJHZ1311, and the State Key Laboratory of Plant Genomics grant 2015B0129-02 to J.-M.Z., and the USA National Science Foundation grant 1508504 and funds from the Center for Plant Science Innovation at the University of Nebraska to J.R.A.
Publisher Copyright:
© 2016 Elsevier Inc.
PY - 2016/10/12
Y1 - 2016/10/12
N2 - The Arabidopsis immune receptor FLS2 and co-receptor BAK1 perceive the bacterial flagellin epitope flg22 to activate plant immunity. To prevent this response, phytopathogenic bacteria deploy a repertoire of effector proteins to perturb immune signaling. However, the effector-induced perturbation is often sensed by the host, triggering another layer of immunity. We report that the Pseudomonas syringae effector HopB1 acts as a protease to cleave immune-activated BAK1. Prior to activation, HopB1 constitutively interacts with FLS2. Upon activation by flg22, BAK1 is recruited to the FLS2-HopB1 complex and is phosphorylated at Thr455. HopB1 then specifically cleaves BAK1 between Arg297 and Gly298 to inhibit FLS2 signaling. Although perturbation of BAK1 is known to trigger increased immune responses in plants, the HopB1-mediated cleavage of BAK1 leads to enhanced virulence, but not disease resistance. This study thus reveals a virulence strategy by which a pathogen effector attacks the plant immune system with minimal host perturbation.
AB - The Arabidopsis immune receptor FLS2 and co-receptor BAK1 perceive the bacterial flagellin epitope flg22 to activate plant immunity. To prevent this response, phytopathogenic bacteria deploy a repertoire of effector proteins to perturb immune signaling. However, the effector-induced perturbation is often sensed by the host, triggering another layer of immunity. We report that the Pseudomonas syringae effector HopB1 acts as a protease to cleave immune-activated BAK1. Prior to activation, HopB1 constitutively interacts with FLS2. Upon activation by flg22, BAK1 is recruited to the FLS2-HopB1 complex and is phosphorylated at Thr455. HopB1 then specifically cleaves BAK1 between Arg297 and Gly298 to inhibit FLS2 signaling. Although perturbation of BAK1 is known to trigger increased immune responses in plants, the HopB1-mediated cleavage of BAK1 leads to enhanced virulence, but not disease resistance. This study thus reveals a virulence strategy by which a pathogen effector attacks the plant immune system with minimal host perturbation.
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U2 - 10.1016/j.chom.2016.09.007
DO - 10.1016/j.chom.2016.09.007
M3 - Article
C2 - 27736646
AN - SCOPUS:84992390396
VL - 20
SP - 504
EP - 514
JO - Cell Host and Microbe
JF - Cell Host and Microbe
SN - 1931-3128
IS - 4
ER -