A Plant Lectin Receptor-like Kinase Phosphorylates the Bacterial Effector AvrPtoB to Dampen Its Virulence in Arabidopsis

文献类型： 外文期刊

第一作者： Xu, Ning

作者： Xu, Ning;Luo, Xuming;Wu, Wei;Xing, Yingying;Liang, Yingbo;Liu, Yanzhi;Liu, Jun;Xu, Ning;Luo, Xuming;Xing, Yingying;Liang, Yingbo;Liu, Yanzhi;Liu, Jun;Wu, Wei;Zou, Huasong;Wei, Hai-Lei

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关键词： Arabidopsis; AvrPtoB; LecRK-IX.2; Pseudomonas syringae; ubiquitination

期刊名称：MOLECULAR PLANT （ 影响因子：13.164； 五年影响因子：16.357 ）

ISSN： 1674-2052

年卷期： 2020 年 13 卷 10 期

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收录情况： SCI

摘要： Plasma membrane-localized receptor-like kinases (RLKs) perceive conserved pathogen-associated molecular patterns (PAMPs) in plants, leading to PAMP-triggered immunity (PTI). The Arabidopsis thaliana lectin RLK LecRK-IX.2 has been shown to regulate the bacterial flagellin-derived peptide flg22-induced PTI. Here, we discover that Pseudomonas syringae effector AvrPtoB targets LecRK-IX.2 for degradation, which subsequently suppresses LecRK-IX.2-mediated PTI and disease resistance. However, LecRK-IX.2 can interact with and phosphorylate AvrPtoB at serine site 335 (S335). AvrPtoB self-associates in vitro and in vivo, and the association appears to be essential for its E3 ligase activity in ubiquitinating substrate in plants. Phosphorylation of S335 disrupts the self-association and as a result, phosphomimetic AvrPtoB(S)(335D) cannot ubiquitinate LecRK-IX.2 efficiently, leading to the compromised virulence of AvrPtoB in suppressing PTI responses. flg22 enhances AvrPtoB S335 phosphorylation by inducing the expression and activating of LecRK-IX.2. Our study demonstrates that host RLKs can modify pathogen effectors to dampen their virulence and undermine their ability in suppressing PTI.

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