A Receptor Pair with an Integrated Decoy Converts Pathogen Disabling of Transcription Factors to Immunity

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Le roux, Clémentine | Huet, Gaëlle | Jauneau, Alain | Camborde, Laurent | Tremousaygue, Dominique | Kraut, Alexandra | Zhou, Binbin | Levaillant, Marie | Adachi, Hiroaki | Yoshioka, Hirofumi | Raffaele, Sylvain | Berthomé, Richard | Couté, Yohann | Parker, Jane, E. | Deslandes, Laurent

Edité par CCSD ; Elsevier -

Comment in Treasure your exceptions: unusual domains in immune receptors reveal host virulence targets. [Cell. 2015]. International audience. Microbial pathogens infect host cells by delivering virulence factors (effectors) that interfere with defenses. In plants, intracellular nucleotide-binding/leucine-rich repeat receptors (NLRs) detect specific effector interference and trigger immunity by an unknown mechanism. The Arabidopsis-interacting NLR pair, RRS1-R with RPS4, confers resistance to different pathogens, including Ralstonia solanacearum bacteria expressing the acetyltransferase effector PopP2. We show that PopP2 directly acetylates a key lysine within an additional C-terminal WRKY transcription factor domain of RRS1-R that binds DNA. This disrupts RRS1-R DNA association and activates RPS4-dependent immunity. PopP2 uses the same lysine acetylation strategy to target multiple defense-promoting WRKY transcription factors, causing loss of WRKY-DNA binding and transactivating functions needed for defense gene expression and disease resistance. Thus, RRS1-R integrates an effector target with an NLR complex at the DNA to switch a potent bacterial virulence activity into defense gene activation.

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