Functional characterisation of a novel semi-dominant mutant allele of the "Chitin Elicitor Receptor-like Kinase" CERK1

“几丁质诱导子受体样激酶”CERK1 的新型半显性突变等位基因的功能表征

• 批准号: 146209784
• 负责人: Professor Dr. Volker Lipka
• 金额: --
• 依托单位: Abteilung Zellbiologie der Pflanze
• 依托单位国家: 德国
• 项目类别: Priority Programmes
• 财政年份: 2009
• 资助国家: 德国
• 起止时间: 2008-12-31 至 2013-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/146209784?language=en
• 关键词: Functional; characterisation; novel; semi; dominant

This project focuses on a novel molecular mechanism that controls cell death execution and containment in plant cells in response to pathogen infection. We have previously identified a novel semi-dominant mutation in the CERK1 gene of Arabidopsis (cerk1-4), which confers enhanced resistance to infection by several biotrophic powdery mildew fungi. Significantly, this resistance is correlated with a deregulated spreading cell death response. This indicates that the plasma-membrane localised receptor-like kinase CERK1, apart from its function in the perception of the fungal PAMP chitin (and a yet unidentified bacterial danger signal) is a regulator of pathogen-induced cell death. Interestingly, intrinsic kinase activity is not required for the cerk1-4 mutant phenotype. Instead, we have shown that aberrant cell death containment in the cerk1-4 mutant correlates with lack of a soluble 33 kDa derivative of the CERK1 protein, which represents the N-terminal ectodomain. In wild-type plants, this ectodomain fragment localises to the apoplast and appears to be the product of controlled enzymatic proteolysis. In vertebrates, tightly regulated shedding of the ectodomain of trans-membrane proteins is a well-established post-translational regulatory mechanism. To our knowledge, ectodomain shedding has not yet been described for plant proteins. The cerk1-4 mutant allele thus represents an excellent entree into understanding ectodomain shedding of plant transmembrane proteins in general and how this regulatory mechanism is involved in plant cell death containment.

该项目的重点是一种新的分子机制，控制细胞死亡的执行和遏制在植物细胞响应病原体感染。我们以前已经确定了一种新的半显性突变的拟南芥（cerk 1 -4），赋予增强的抗感染的几个活体营养型白粉病真菌的CERK 1基因。值得注意的是，这种抗性与失调的扩散细胞死亡反应相关。这表明质膜定位的受体样激酶CERK 1，除了其在真菌PAMP几丁质（和尚未鉴定的细菌危险信号）的感知中的功能外，是病原体诱导的细胞死亡的调节剂。有趣的是，cerk 1 -4突变表型不需要内在激酶活性。相反，我们已经表明，异常的细胞死亡遏制在cerk 1 -4突变体与缺乏一个可溶性的33 kDa的衍生物的CERK 1蛋白，这代表了N-末端胞外域。在野生型植物中，该胞外域片段定位于质外体，并且似乎是受控酶促蛋白水解的产物。在脊椎动物中，跨膜蛋白的胞外结构域的严格调控的脱落是一种完善的翻译后调节机制。据我们所知，胞外结构域脱落尚未被描述为植物蛋白。因此，cerk 1 -4突变等位基因代表了一个很好的入门了解胞外区脱落的植物跨膜蛋白一般和这种调节机制是如何参与植物细胞死亡遏制。