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Wiley InterScience | ||
![]() The Plant JournalVolume 50 Issue 3, Pages 488 - 499 Published Online: 5 Apr 2007 Journal compilation © 2010 Blackwell Publishing Ltd and the Society for Experimental Biology Published in association with the Society for Experimental Biology
Abstract | References | Full Text: HTML, PDF (Size: 824K) | Supporting Information | Related Articles | Citation Tracking Overexpression of CRK13, an Arabidopsis cysteine-rich receptor-like kinase, results in enhanced resistance to Pseudomonas syringae Copyright 2007 The Authors Journal compilation 2007 Blackwell Publishing Ltd KEYWORDS cysteine-rich receptor-like kinase • salicylic acid • pathogen defense • Arabidopsis • signaling • cell death ABSTRACTProtein kinases play important roles in relaying information from perception of a signal to the effector genes in all organisms. Cysteine-rich receptor-like kinases (CRKs) constitute a sub-family of plant receptor-like kinases (RLKs) with more than 40 members that contain the novel C-X8-C-X2-C motif (DUF26) in the extracellular domains. Here we report molecular characterization of one member of this gene family, CRK13. Expression of this gene is induced more quickly and strongly in response to the avirulent compared with the virulent strains of Pseudomonas syringae, and peaks within 4 h after pathogen infection. In response to dexamethasone (DEX) treatment, plants expressing the CRK13 gene from a DEX-inducible promoter exhibited all tested features of pathogen defense activation, including rapid tissue collapse, accumulation of high levels of several defense-related gene transcripts including PR1, PR5 and ICS1, and accumulation of salicylic acid (SA). In addition, these plants suppressed growth of virulent pathogens by about 20-fold compared with the wild-type Col-0. CRK13-conferred pathogen resistance is salicylic acid-dependent. Gene expression analysis using custom cDNA microarrays revealed a remarkable overlap between the expression profiles of the plants overexpressing CRK13 and the plants treated with Pst DC3000 (avrRpm1). Our studies suggest that upregulation of CRK13 leads to hypersensitive response-associated cell death, and induces defense against pathogens by causing increased accumulation of salicylic acid. Received 31 October 2006; revised 19 December 2006; accepted 10 January 2007. |