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A novel Arabidopsis CHITIN ELICITOR RECEPTOR KINASE 1 (CERK1) mutant with enhanced pathogen‐induced cell death and altered receptor processing
- Petutschnig, Elena K., Stolze, Marnie, Lipka, Ulrike, Kopischke, Michaela, Horlacher, Juliane, Valerius, Oliver, Rozhon, Wilfried, Gust, Andrea A., Kemmerling, Birgit, Poppenberger, Brigitte, Braus, Gerhard H., Nürnberger, Thorsten, Lipka, Volker
- The new phytologist 2014 v.204 no.4 pp. 955-967
- Arabidopsis, alleles, amino acids, animals, barley, cell death, chitin, crossing, elicitors, mutants, mutation, pathogens, phenotype, powdery mildew, receptors, salicylic acid, surface proteins
- Plants detect pathogens by sensing microbe‐associated molecular patterns (MAMPs) through pattern recognition receptors. Pattern recognition receptor complexes also have roles in cell death control, but the underlying mechanisms are poorly understood. Here, we report isolation of cerk1‐4, a novel mutant allele of the Arabidopsis chitin receptor CERK1 with enhanced defense responses. We identified cerk1‐4 in a forward genetic screen with barley powdery mildew and consequently characterized it by pathogen assays, mutant crosses and analysis of defense pathways. CERK1 and CERK1‐4 proteins were analyzed biochemically. The cerk1‐4 mutation causes an amino acid exchange in the CERK1 ectodomain. Mutant plants maintain chitin signaling capacity but exhibit hyper‐inducible salicylic acid concentrations and deregulated cell death upon pathogen challenge. In contrast to chitin signaling, the cerk1‐4 phenotype does not require kinase activity and is conferred by the N‐terminal part of the receptor. CERK1 undergoes ectodomain shedding, a well‐known process in animal cell surface proteins. Wild‐type plants contain the full‐length CERK1 receptor protein as well as a soluble form of the CERK1 ectodomain, whereas cerk1‐4 plants lack the N‐terminal shedding product. Our work suggests that CERK1 may have a chitin‐independent role in cell death control and is the first report of ectodomain shedding in plants.