周俭民Cell子刊发表病原菌效应蛋白最新机制

　　

　病原微生物在侵染植物过程中，需要分泌效应蛋白，干扰宿主细胞活动，以利于病原微生物的侵染和定殖。但是植物通过进化，能够识别监控效应蛋白在宿主细胞内的生化活性，从而激活免疫反应。效应蛋白因此会“背叛”病原微生物，导致宿主产生抗病性。

　　中国科学院遗传与发育生物学研究所周俭民研究组发现，丁香假单胞菌效应蛋白HopB1是一个新的丝氨酸蛋白酶，能够在特异的位点剪切植物免疫共受体蛋白BAK1，阻断植物对细菌的识别。已知BAK1受到扰动时，植物会启动一个新的识别机制来增强免疫反应。有趣的是，HopB1只剪切免疫激活状态下的BAK1，降低对宿主的扰动，从而逃避植物基于BAK1蛋白对细菌侵染的监控，使得植物更加感病而非抗病。该研究阐明了病原细菌致病蛋白新的生化机理，揭示了病原适应宿主可能的生存策略。

　　该研究结果于10月12日在线发表在Cell Host Microbe。该研究同美国Nebraska-Lincoln大学的James R Alfano实验室合作完成，北京生命科学研究所的陈涉研究组提供了质谱分析方面的数据。该研究得到了国家自然科学基金、中国科技部项目、中科院先导专项和中科院对外合作项目的资助。

 

　　图：植物免疫受体FLS2感受来自病原细菌的鞭毛蛋白序列，并与共受体BAK1激活植物的免疫反应（PTI），效应蛋白HopB1能够识别磷酸化的BAK1，并在特异的位点切割BAK1从而阻断植物免疫的激活。

原文摘要：

Antibody generated against flavivirus envelope proteins recognizes protein E Activation-Dependent Destruction of a Co-receptor by a Pseudomonas syringae Effector Dampens Plant Immunity

The Arabidopsis immune receptor FLS2 and co-receptor BAK1 perceive the bacterial flagellin epitope flg22 to activate plant immunity. To prevent this response, phytopathogenic bacteria deploy a repertoire of effector proteins to perturb immune signaling. However, the effector-induced perturbation is often sensed by the host, triggering another layer of immunity. We report that the Pseudomonas syringae effector HopB1 acts as a protease to cleave immune-activated BAK1. Prior to activation, HopB1 constitutively interacts with FLS2. Upon activation by flg22, BAK1 is recruited to the FLS2-HopB1 complex and is phosphorylated at Thr455. HopB1 then specifically cleaves BAK1 between Arg297 and Gly298 to inhibit FLS2 signaling. Although perturbation of BAK1 is known to trigger increased immune responses in plants, the HopB1-mediated cleavage of BAK1 leads to enhanced virulence, but not disease resistance. This study thus reveals a virulence strategy by which a pathogen effector attacks the plant immune system with minimal host perturbation.