Zhang Jie, Shao Feng, Li Yan, Cui Haitao, Chen Linjie, Li Hongtao, Zou Yan, Long Chengzu, Lan Lefu, Chai Jijie, Chen She, Tang Xiaoyan, Zhou Jian-Min
National Key Laboratory of Plant Molecular Genetics, Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200032, China.
Cell Host Microbe. 2007 May 17;1(3):175-85. doi: 10.1016/j.chom.2007.03.006.
Pathogen-associated molecular patterns (PAMPs) elicit basal defense responses in plants, and, in turn, pathogens have evolved mechanisms to overcome these PAMP-induced defenses. To suppress immunity, the phytopathogenic bacterium Pseudomonas syringae secretes effector proteins, the biochemical function and virulence targets of which remain largely unknown. We show that HopAI1, an effector widely conserved in both plant and animal bacterial pathogens, inhibits the Arabidopsis mitogen-activated protein kinases (MAPKs) activated by exposure to PAMPs. HopAI1 inactivates MAPKs by removing the phosphate group from phosphothreonine through a unique phosphothreonine lyase activity, which is required for HopAI1 function. The inhibition of MAPKs by HopA1 suppresses two independent downstream events, namely the reinforcement of cell wall defense and transcriptional activation of PAMP response genes. The MAPKs MPK3 and MPK6 physically interact with HopAI1 indicating that they are direct targets of HopAI1. These findings uncover a mechanism by which Pseudomonas syringae overcomes host innate immunity to promote pathogenesis.
病原体相关分子模式（PAMPs）引发植物的基础防御反应，反过来，病原体也进化出了克服这些由PAMPs诱导的防御机制。为了抑制免疫反应，植物致病细菌丁香假单胞菌分泌效应蛋白，但其生化功能和毒力靶点在很大程度上仍不清楚。我们发现，HopAI1是一种在植物和动物细菌病原体中广泛保守的效应蛋白，它能抑制拟南芥中因暴露于PAMPs而激活的丝裂原活化蛋白激酶（MAPKs）。HopAI1通过一种独特的磷酸苏氨酸裂解酶活性从磷酸苏氨酸上去除磷酸基团，从而使MAPKs失活，这是HopAI1发挥功能所必需的。HopA1对MAPKs的抑制作用抑制了两个独立的下游事件，即细胞壁防御的增强和PAMP反应基因的转录激活。MAPKs MPK3和MPK6与HopAI1发生物理相互作用，表明它们是HopAI1的直接靶点。这些发现揭示了丁香假单胞菌克服宿主先天免疫以促进发病的一种机制。
