Direct acetylation of a conserved threonine of RIN4 by the bacterial effector HopZ5 or AvrBsT activates RPM1-dependent immunity in Arabidopsis.

ABSTRACT

Plant pathogenic bacteria deliver effectors into plant cells to suppress immunity and promote pathogen survival; however, these effectors can be recognized by plant disease resistance proteins to activate innate immunity. The bacterial acetyltransferase effectors HopZ5 and AvrBsT trigger immunity in Arabidopsis thaliana genotypes lacking SUPPRESSOR OF AVRBST-ELICITED RESISTANCE 1 (SOBER1). Using an Arabidopsis accession, Tscha-1, that naturally lacks functional SOBER1 but is unable to recognize HopZ5, we demonstrated that RESISTANCE TO P. SYRINGAE PV MACULICOLA 1 (RPM1) and RPM1-INTERACTING PROTEIN 4 (RIN4) are indispensable for HopZ5- or AvrBsT-triggered immunity. Remarkably, T166 of RIN4, the phosphorylation of which is induced by AvrB and AvrRpm1, is directly acetylated by HopZ5 and AvrBsT. Furthermore, we demonstrated that the acetylation of RIN4 T166 is required and sufficient for HopZ5- or AvrBsT-triggered RPM1-dependent defense activation. Finally, we showed that SOBER1 interferes with HopZ5- or AvrBsT-triggered immunity by deacetylating RIN4 T166. Collectively, our study elucidates detailed molecular mechanisms underlying the activation and suppression of plant innate immunity triggered by two bacterial acetyltransferases, HopZ5 and AvrBsT, from different bacterial pathogens.