Plants detect microbes via two functionally intercon-nected tiers of immune receptors. Immune detectionis suppressed by equally complex pathogen mecha-nisms. The small plasma-membrane-tethered pro-tein RIN4 negatively regulates microbe-associatedmolecular pattern (MAMP)-triggered responses, whichare derepressed upon bacterial flagellin perception.We demonstrate that recognition of the flagellinpeptide MAMP flg22 triggers accumulation of RIN4phosphorylated at serine 141 (pS141) that mediatesderepression of several immune outputs. RIN4 istargeted by four bacterial type III effector proteins,delivered temporally after flagellin perception. Ofthese, AvrB acts with a host kinase to increase levelsof RIN4 phosphorylated at threonine 166 (pT166).RIN4 pT166 is epistatic to RIN4 pS141. Thus, AvrBcontributes to virulence by enhancing "rerepression" of immune system outputs. Our results explain theevolution of independent effectors that antagonizeaccumulation of RIN4 pS141 and of a specific plantintracellular NLR protein, RPM1, which is activatedby AvrB-mediated accumulation of RIN4 pT166.
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