Chitin-Induced Dimerization Activates a Plant Immune Receptor
Chitin-Induced Dimerization Activates a Plant Immune Receptor
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甲壳素诱导的二聚化激活植物免疫受体
DOI：
10.1126/science.1218867
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发表时间：
2012-06-01
期刊：
影响因子：
56.9
通讯作者：
Chai, Jijie
中科院分区：
文献类型：
--
作者：
Liu, Tingting;Liu, Zixu;Chai, Jijie
模式识别受体通过识别保守的病原体相关分子模式赋予植物对病原体感染的抗性。拟南芥的细胞表面受体几丁质激发子受体激酶1（AtCERK 1）通过其含有赖氨酸基序（LysM）的胞外域（AtCERK 1-ECD）直接结合几丁质以激活免疫应答。我们解决的AtCERK 1-ECD与几丁质五聚体复合的晶体结构揭示了它们的相互作用主要由LysM和三个几丁质残基介导。通过充当二价配体，几丁质八聚体诱导AtCERK 1-ECD二聚化，所述AtCERK 1-ECD二聚化被较短的几丁质寡聚体抑制。一种突变减弱几丁质诱导的AtCERK 1-ECD二聚化或通过AtCERK 1-ECD过表达形成非生产性AtCERK 1二聚体，这损害了植物细胞中AtCERK 1介导的信号传导。总之，我们的数据支持的概念，几丁质诱导AtCERK 1二聚化是其激活的关键。
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.