Graduate Program in Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Science. 2012 Jun 1;336(6085):1160-4. doi: 10.1126/science.1218867.
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.
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。拟南芥细胞表面受体几丁质激发受体激酶 1（AtCERK1）通过其含有赖氨酸基序（LysM）的胞外结构域（AtCERK1-ECD）直接与几丁质结合，从而激活免疫反应。我们解决的一个 AtCERK1-ECD 与五聚体几丁质复合物的晶体结构揭示了它们的相互作用主要是由一个 LysM 和三个几丁质残基介导的。作为一个二价配体，一个八聚体几丁质诱导 AtCERK1-ECD 二聚化，而较短的几丁质低聚物抑制这种二聚化。通过过表达 AtCERK1-ECD 来减弱几丁质诱导的 AtCERK1-ECD 二聚化或形成非生产性 AtCERK1 二聚体的突变，会损害 AtCERK1 介导的植物细胞信号转导。总之，我们的数据支持这样的观点，即几丁质诱导的 AtCERK1 二聚化对于其激活至关重要。
