茉莉酸
生物
NPR1
拟南芥
植物免疫
转录因子
细胞生物学
拟南芥
丁香假单胞菌
信号转导
效应器
水杨酸
生物化学
基因
利钠肽
突变体
心力衰竭
内科学
医学
作者
Hongqing Guo,Trevor M. Nolan,Gaoyuan Song,Sanzhen Liu,Zhouli Xie,Jiani Chen,Patrick S. Schnable,Justin W. Walley,Yanhai Yin
出处
期刊:Current Biology
[Elsevier]
日期:2018-10-01
卷期号:28 (20): 3316-3324.e6
被引量:171
标识
DOI:10.1016/j.cub.2018.07.078
摘要
Bacterial pathogens use effectors and phytotoxins to facilitate infection of host plants. Coronatine (COR) is one of the phytotoxins produced in bacterial pathogens, such as Pseudomonas syringae pv. tomato DC3000 (pst DC3000). COR structurally and functionally mimics the active form of the plant hormone jasmonic acid (JA), JA-isoleucine (JA-Ile), and can hijack the host JA-signaling pathway to achieve host disease susceptibility [1]. COR utilizes the transcription factor MYC2, a master regulator of JA signaling, to activate NAC transcription factors, which functions to inhibit accumulation of salicylic acid (SA) and thus compromise host immunity [2]. It has been demonstrated that SA can antagonize JA signaling through NONEXPRESSOR of PATHOGENESIS-RELATED GENE1 (NPR1) [3] and downstream transcription factors TGAs [4] and WRKYs [5, 6]. However, the detailed mechanism by which host plants counteract COR-mediated susceptibility is largely unknown. Here, we show that the receptor kinase FERONIA (FER) functions to inhibit JA and COR signaling by phosphorylating and destabilizing MYC2, thereby positively regulating immunity. Conversely, the peptide ligand RALF23 acts through FER to stabilize MYC2 and elevate JA signaling, negatively contributing to plant immunity. Our results establish the RALF23-FER-MYC2 signaling module and provide a previously unknown mechanism by which host plants utilize FER signaling to counteract COR-mediated host disease susceptibility.
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