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Science:周俭民等植物天然免疫机制研究获进展

2012-07-03 遗传与发育生物学研究所 遗传与发育生物学研究所

植物天然免疫机制研究取得重要进展 植物的天然免疫是植物免疫系统的重要组成部分。在植物的细胞膜上存在多种模式识别受体,通过识别病原体上的一些共有的、保守的分子基序(也即病原相关分子模式),引发先天免疫反应。真菌病原体细胞壁的主要组分几丁质是β-1,4连接的N –乙酰氨基葡萄糖的多聚物,可以作为一种病原分子相关模式刺激植物产生免疫反应。几丁质在拟南芥中的受体CERK1是一种LysM类型的受体激酶,胞

植物天然免疫机制研究取得重要进展

植物的天然免疫是植物免疫系统的重要组成部分。在植物的细胞膜上存在多种模式识别受体,通过识别病原体上的一些共有的、保守的分子基序(也即病原相关分子模式),引发先天免疫反应。真菌病原体细胞壁的主要组分几丁质是β-1,4连接的N –乙酰氨基葡萄糖的多聚物,可以作为一种病原分子相关模式刺激植物产生免疫反应。几丁质在拟南芥中的受体CERK1是一种LysM类型的受体激酶,胞外含有三个串联的LysM结构域。已有的研究结果表明,体外表达纯化的CERK1能直接结合几丁质,但是其识别几丁质的分子机制和结合几丁质后的激活机制却亟待阐明。

中科院遗传与发育生物学研究所周俭民研究组与清华大学的柴继杰研究组等合作,通过多种生化和功能分析以及结构生物学实验,发现了几丁质激活CERK1的机理。结果表明:当植物宿主细胞感受到几丁质时,植物细胞膜上的AtCERK1通过胞外LysM结构域二聚化来完成配体感应,使其胞内结构域磷酸化并激活下游防卫反应信号通路。

该项研究为理解植物免疫调控及其它受体激酶的作用方式提供了一个宝贵的模型。

该项工作于6月1日以Chitin-Induced Dimerization Activates a Plant Immune Receptor为题,在Science杂志发表(336:1160-1164)。柴继杰教授、周俭民研究员和郑州大学常俊标教授为共同通讯作者;柴继杰指导的研究生刘婷婷和周俭民指导的研究生刘自旭为共同第一作者;来自北京大学的研究人员也参与了部分研究工作。

该项研究得到了科技部的资助。

doi:10.1126/science.1218867
PMC:
PMID:

Chitin-Induced Dimerization Activates a Plant Immune Receptor

Tingting Liu1,2,3,4,*, Zixu Liu4,5,*, Chuanjun Song6, Yunfei Hu7,8, Zhifu Han2,3, Ji She8, Fangfang Fan6, Jiawei Wang3, Changwen Jin7,8, Junbiao Chang6,†, Jian-Min Zhou4,9,†, Jijie Chai2,3,†

Pattern recognition receptors confer plant resistance to pathogen infection by recognizing the conserved pathogen-associated molecular patterns. The cell surface receptor chitin elicitor receptor kinase 1 of Arabidopsis (AtCERK1) directly binds chitin through its lysine motif (LysM)–containing ectodomain (AtCERK1-ECD) to activate immune responses. The crystal structure that we solved of an AtCERK1-ECD complexed with a chitin pentamer reveals that their interaction is primarily mediated by a LysM and three chitin residues. By acting as a bivalent ligand, a chitin octamer induces AtCERK1-ECD dimerization that is inhibited by shorter chitin oligomers. A mutation attenuating chitin-induced AtCERK1-ECD dimerization or formation of nonproductive AtCERK1 dimer by overexpression of AtCERK1-ECD compromises AtCERK1-mediated signaling in plant cells. Together, our data support the notion that chitin-induced AtCERK1 dimerization is critical for its activation.

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    2012-07-05 jichang
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