Choi Sera, Prokchorchik Maxim, Lee Hyeonjung, Gupta Ravi, Lee Yoonyoung, Chung Eui-Hwan, Cho Buhyeon, Kim Min-Sung, Kim Sun Tae, Sohn Kee Hoon
Department of Life Sciences, Pohang University of Science and Technology, Pohang 37673, Republic of Korea.
Department of Plant Bioscience, Life and Industry Convergence Research Institute, Pusan National University, Miryang 50463, Republic of Korea; Department of Botany, School of Chemical and Life Sciences, Jamia Hamdard, Hamdard Nagar, New Delhi 110062, India.
Mol Plant. 2021 Nov 1;14(11):1951-1960. doi: 10.1016/j.molp.2021.07.017. Epub 2021 Jul 27.
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.
植物病原细菌将效应蛋白输送到植物细胞中以抑制免疫并促进病原体存活；然而，这些效应蛋白可被植物抗病蛋白识别以激活先天免疫。细菌乙酰转移酶效应蛋白HopZ5和AvrBsT在缺乏AVRBST诱导抗性抑制因子1（SOBER1）的拟南芥基因型中触发免疫。利用一种天然缺乏功能性SOBER1但无法识别HopZ5的拟南芥生态型Tscha-1，我们证明了对丁香假单胞菌番茄致病变种1（P. syringae pv maculicola 1）的抗性（RPM1）和RPM1相互作用蛋白4（RIN4）对于HopZ5或AvrBsT触发的免疫是不可或缺的。值得注意的是，RIN4的T166位点，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RIN4 T166的乙酰化对于HopZ5或AvrBsT触发的依赖RPM1的防御激活是必需且充分的。最后，我们表明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。
