Abstract：
Pathogens generate and secrete effector proteins to the host plant cells during pathogenesis to promote virulence and colonization. If the plant carries resistance (R) proteins that recognize pathogen effectors, effector-triggered immunity (ETI) is activated, resulting in a robust immune response and hypersensitive response (HR). The bipartite effector AvrRps4 from Pseudomonas syringae pv. pisi has been well studied in terms of avirulence function. In planta, AvrRps4 is processed into two parts. The C-terminal fragment of AvrRps4 (AvrRps4C) induces HR in turnip and is recognized by the paired resistance proteins AtRRS1/AtRPS4 in Arabidopsis. Here, we show that AvrRps4C targets a group of Arabidopsis WRKY, including WRKY46, WRKY53, WRKY54, and WRKY70, to induce its virulence function. Indeed, AvrRps4C suppresses the general binding and transcriptional activities of immune-positive regulator WRKY54 and WRKY54-mediated resistance. AvrRps4C interferes with WRKY54\'s binding activity to target gene SARD1 in vitro, suggesting WRKY54 is sequestered from the SARD1 promoter by AvrRps4C. Through the interaction of AvrRps4C with four WRKYs, AvrRps4 enhances the formation of homo-/heterotypic complexes of four WRKYs and sequesters them in the cytoplasm, thus inhibiting their function in plant immunity. Together, our results provide a detailed virulence mechanism of AvrRps4 through its C-terminus.
摘要：
病原体在发病过程中产生并分泌效应蛋白到宿主植物细胞以促进毒力和定殖。如果植物携带识别病原体效应子的抗性（R）蛋白，效应子触发免疫（ETI）被激活，导致强大的免疫反应和过敏反应（HR）。来自丁香假单胞菌pv的二分效应子AvrRps4。pisi在无毒功能方面已经得到了很好的研究。在植物中,AvrRps4被处理成两个部分。AvrRps4的C端片段（AvrRps4C）在萝卜中诱导HR，并被拟南芥中的配对抗性蛋白AtRRS1/AtRPS4识别。这里,我们显示AvrRps4C靶向一组拟南芥WRKY，包括WRKY46，WRKY53，WRKY54和WRKY70，以诱导其毒力功能。的确,AvrRps4C抑制免疫阳性调节因子WRKY54和WRKY54介导的抗性的一般结合和转录活性。AvrRps4C在体外干扰WRKY54与靶基因SARD1的结合活性，表明WRKY54通过AvrRps4C与SARD1启动子隔离。通过AvrRps4C与四个WRKY的相互作用，AvrRps4增强了四个WRKYs的同型/异型复合物的形成，并将它们隔离在细胞质中，从而抑制它们在植物免疫中的功能。一起,我们的结果提供了AvrRps4通过其C末端的详细毒力机制。
