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

点击翻译按钮获取中文摘要

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.