植物致病性细菌通过III型分泌系统向寄主细胞中注射效应蛋白，来抑制寄主的免疫反应或干扰细胞正常的生理功能，促进细菌的侵染。III型效应蛋白通常靶向寄主的蛋白质或者DNA，然而，目前尚未有III型效应蛋白靶向寄主RNA的报道。青枯病菌是一种世界范围内毁灭性的植物病原细菌，前期的序列分析发现青枯病菌中的III型效应蛋白RipL具有PPR类RNA结合功能域，但其寄主靶标及促进细菌侵染的分子机制还不清楚。本项目拟研究（1）RipL对青枯病菌致病力的影响及其亚细胞定位；（2）综合运用一系列遗传、分子、生化及生物信息手段，分离鉴定RipL在寄主体内的靶标RNA并阐明其作用机制；（3）通过基因编辑等手段，探索RipL寄主靶标促进病害发生的分子机理。本项目不仅将首次认识细菌III型效应蛋白在调节寄主RNA方面的新的分子功能，还将促进对青枯病菌与寄主互作的分子机制的理解，为该病的抗病育种提供新的理论基础。

Plant pathogenic bacteria use a type III secretion system to inject effector proteins into host cells, which suppress plant immunity or interfere with cellular functions promoting infection. Type III effectors normally target host protein or DNA, however, till so far it is unclear if type III effectors could target host RNA. Ralstonia solanacearum is one of the devastating phytopathogenic bacteria across the world. Previous sequence analysis revealed that the type III effector RipL from R. solanacearum has PPR-type RNA binding motif. Yet, the host target of RipL and the molecular mechanism on how the target promotes infection remain unknown. This study aims to (1) investigate the virulence contribution of RipL and its subcellular localization, (2) identify the host target RNA of RipL by using combined genetic, molecular, biochemical and bioinformatic approaches, and study its action mechanism, (3) characterize the molecular mechanism on how RipL targeted host gene promotes disease. This study will, for the first time, help to recognize the molecular function of bacterial type III effectors in regulating host RNA. Furthermore, this study will help us to better understand the molecular interaction between R. solanacearum and its host plants and provide theoretical evidence for resistant breeding against bacterial wilt.