How does pathogen perception via the WRKY domain activate the RRS1/RPS4 immune complex? 
Y. MA (1), P. Martinez (1), . Duxbury (2), P. Sarris (3), H. Brown (1), L. Wirthmueller (4), J. Jones (1) (1) The Sainsbury Laboratory, United Kingdom; (2) The Sainsbury Laboratory, United Kingdom; (3) University of Exeter, United Kingdom; (4) University of Berlin, Germany

Central to plant survival is the ability to activate immunity upon pathogen perception. Plants deploy immune receptors (NLRs) to recognize specific pathogen molecules (effectors) and to trigger defense. These receptors usually recognize a specific effector, but some work in pairs and can detect multiple effectors. How receptor complexes operate to convert effector perception into defense activation is poorly understood. The Arabidopsis RPS4/RRS1 receptor pair detects two distinct effectors that target WRKY transcription factors via an integrated WRKY domain of RRS1. My work aims to unravel the perplexing intra- and inter-domain reconfigurations that convert effector/WRKY interactions into complex activation. We found deletion of RRS1 WRKY domain constitutively activates RPS4. This indicates the complex is activated by effector-dependent release of negative regulation from the WRKY domain. Co-IP shows effector AvrRps4 disrupts WRKY association with the nearby 4th domain (DOM4) of RRS1. How then does RRS1 relay the signal to activate RPS4? Domain swaps analysis between RRS1/RPS4 and related RRS1B/RPS4B reveals key interactions required for activation, notably between DOM4 of RRS1 and C-terminal domain (CTD) of RPS4. Recent observations suggest distinct CTD/DOM4 interfaces may be specifically required for activation by different effectors. Such mechanistic insights of complex autoinhibition and activation would provide valuable knowledge for future immune receptor engineering.    

Abstract Number: P17-566
Session Type: Poster