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.

植物病原菌将效应子传递到植物细胞中，抑制免疫力，促进病原体存活；然而，这些效应子可以被植物抗病蛋白识别，从而激活先天免疫。细菌乙酰转移酶效应子 HopZ5 和 AvrBsT 在缺乏AVRBST 诱导抗性抑制因子 1 ( SOBER1 )的拟南芥基因型中引发免疫。使用天然缺乏功能性SOBER1但无法识别 HopZ5 的拟南芥属植物Tscha-1 ，我们证明了对丁香假单胞菌 PV MACULICOLA 1 ( RPM1 ) 和RPM1-相互作用蛋白4 ( RIN4 ) 的抗性) 对于 HopZ5 或 AvrBsT 触发的免疫是必不可少的。值得注意的是，RIN4 的 T166，其磷酸化由 AvrB 和 AvrRpm1 诱导，被 HopZ5 和 AvrBsT 直接乙酰化。此外，我们证明了 RIN4 T166 的乙酰化对于 HopZ5 或 AvrBsT 触发的 RPM1 依赖性防御激活是必需且足够的。最后，我们发现 SOBER1 通过使 RIN4 T166 去乙酰化来干扰 HopZ5 或 AvrBsT 触发的免疫。总的来说，我们的研究阐明了由来自不同细菌病原体的两种细菌乙酰转移酶 HopZ5 和 AvrBsT 触发的植物先天免疫激活和抑制的详细分子机制。