生物谷報道：2007年5月16日，周儉民研究小組在Cell Host & Microbe上發(fā)表了題為 “A Pseudomonas syringae Effector Inactivates MAPKs to Suppress PAMP-Induced Immunity in Plants” 的論文,，報道了他們關(guān)于假單胞桿菌效應(yīng)蛋白致病機理的新發(fā)現(xiàn),。
假單胞桿菌三型分泌系統(tǒng)分泌的效應(yīng)蛋白是毒性假單胞桿菌最重要的致病武器，但是目前對這些效應(yīng)蛋白的生化功能和它們在宿主體內(nèi)的直接作用位點還知之甚少,。該論文報道假單胞桿菌Pseudomonas syringae pv. tomato DC3000的效應(yīng)蛋白HopAI1能夠廣泛抑制植物先天免疫反應(yīng),，并證明擬南芥絲裂原活化蛋白激酶（MAPK, Mitogen-activated protein kinase）MPK3和MPK6是HopAI1在植物體內(nèi)的直接毒性靶位點。HopAI1屬于一個在植物和動物病原菌中廣泛存在并且保守的效應(yīng)蛋白家族,，HopAI1能直接與擬南芥MPK3和MPK6相互作用,，并通過獨特的磷酸化蘇氨酸裂解酶活性使其去磷酸化并失活，揭示了細(xì)菌抑制宿主防衛(wèi)反應(yīng)的一個新的作用機制,。同時該研究還分析了MAPK下游信號途徑,，表明MAPK通過激活與活性氧調(diào)節(jié)細(xì)胞壁防衛(wèi)反應(yīng)。
博士生張杰為本論文第一作者,，論文的其他作者還有邵峰博士,、柴繼杰博士,、李燕、崔海濤,、陳琳潔,、李洪濤博士、鄒燕,、蛋白質(zhì)中心的龍承租和陳涉,，以及堪薩斯州立大學(xué)的蘭樂夫博士和唐曉艷博士。周儉民博士為本文通訊作者,。
該項目由科技部863項目和北京市政府資助,。
原始出處:
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
[email protected]
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.
全文鏈接：http://www.cellhostandmicrobe.com/content/article/fulltext?uid=PIIS1931312807000455
