生物谷报道：2007年5月16日，周俭民研究小组在Cell Host & Microbe上发表了题为 “A Pseudomonas syringae Effector Inactivates MAPKs to Suppress PAMP-Induced Immunity in Plants” 的论文，报道了他们关于假单胞杆菌效应蛋白致病机理的新发现。
假单胞杆菌三型分泌系统分泌的效应蛋白是毒性假单胞杆菌最重要的致病武器，但是目前对这些效应蛋白的生化功能和它们在宿主体内的直接作用位点还知之甚少。该论文报道假单胞杆菌Pseudomonas syringae pv. tomato DC3000的效应蛋白HopAI1能够广泛抑制植物先天免疫反应，并证明拟南芥丝裂原活化蛋白激酶（MAPK, Mitogen-activated protein kinase）MPK3和MPK6是HopAI1在植物体内的直接毒性靶位点。HopAI1属于一个在植物和动物病原菌中广泛存在并且保守的效应蛋白家族，HopAI1能直接与拟南芥MPK3和MPK6相互作用，并通过独特的磷酸化苏氨酸裂解酶活性使其去磷酸化并失活，揭示了细菌抑制宿主防卫反应的一个新的作用机制。同时该研究还分析了MAPK下游信号途径，表明MAPK通过激活与活性氧调节细胞壁防卫反应。
博士生张杰为本论文第一作者，论文的其他作者还有邵峰博士、柴继杰博士、李燕、崔海涛、陈琳洁、李洪涛博士、邹燕、蛋白质中心的龙承租和陈涉，以及堪萨斯州立大学的兰乐夫博士和唐晓艳博士。周俭民博士为本文通讯作者。
该项目由科技部863项目和北京市政府资助。
原始出处:
Cell Host and Microbe, Vol 1, 175-185, 17 May 2007
Article
A Pseudomonas syringae Effector Inactivates MAPKs to Suppress PAMP-Induced Immunity in Plants
Jie Zhang,1,3 Feng Shao,3 Yan Li,3 Haitao Cui,3 Linjie Chen,3 Hongtao Li,3 Yan Zou,3 Chengzu Long,3 Lefu Lan,2 Jijie Chai,3 She Chen,3 Xiaoyan Tang,2 and Jian-Min Zhou3,
1 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
2 Department of Plant Pathology, Kansas State University, Manhattan, KS 66506, USA
3 National Institute of Biological Sciences, Beijing 102206, China
Corresponding author
Jian-Min Zhou
zhoujianmin@nibs.ac.cn
Summary
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.
全文链接：http://www.cellhostandmicrobe.com/content/article/fulltext?uid=PIIS1931312807000455
