效应器
毒力
诱饵
MAPK/ERK通路
细胞生物学
生物
大丽花黄萎病
拟南芥
激酶
免疫系统
蛋白激酶A
免疫
病菌
信号转导
微生物学
MAPK级联
丝裂原活化蛋白激酶
拟南芥
植物免疫
真菌蛋白
磷酸化
真菌
寄主(生物学)
丁香假单胞菌
遗传筛选
转基因
底物水平磷酸化
蛋白激酶结构域
作者
Xiu-qi Liu,Liu Xian-ping,Lin Jin,Min Luo,Yu-jia Tang,Yu-zhuo Yan,Cheng‐Guo Duan,Chen Zhu
标识
DOI:10.1073/pnas.2603182123
摘要
Plant immune responses rely on mitogen-activated protein kinase (MAPK) cascade that integrates pattern-triggered immunity and effector-triggered immunity. How fungal pathogens suppress this central signaling hub remains poorly understood. Here, we identify a secreted effector from phytopathogenic fungus Verticillium dahliae , VdHCE1, that is required for full virulence and directly targets host MAPK signaling. VdHCE1 interacts with the MAPK kinase MKK5 and is phosphorylated at threonine 166 in planta. Biochemical analyses demonstrated that VdHCE1 competes with MPK3 and MPK6 as a substrate of MKK5, thereby attenuating downstream MAPK activation. Consistently, VdHCE1 suppresses elicitor- and NLR-triggered immune responses, while deletion of VdHCE1 compromises fungal virulence in Arabidopsis and cotton. Genetic disruption of MKK5 restores the virulence of VdHCE1-deficient strains, establishing MKK5 as the functional target of VdHCE1. These findings reveal a strategy by which a filamentous fungal pathogen suppresses plant immunity by acting as a decoy substrate within the MAPK cascade and provide a molecular framework for engineering resistance to vascular wilt disease.
科研通智能强力驱动
Strongly Powered by AbleSci AI