由茄科劳尔氏菌引起的植物细菌性青枯病是一类世界性广泛分布、危害严重的毁灭性维管束病害，缺乏安全有效的防治方法和稳定广谱的抗病资源。植物依赖先天免疫系统抵御病原菌的侵染，病原细菌利用III型分泌系统相关效应蛋白抑制寄主免疫反应，对于如何干扰植物免疫基因诱导表达的认知有限。申请人前期发现了植物细胞核定位的青枯菌效应蛋白RsNE2能够显著抑制寄主免疫基因表达，该蛋白和植物重要的抗病转录因子TGAs相互作用，预示着病原细菌通过劫持转录因子抑制免疫反应的新机制。本项目将系统研究RsNE2在青枯菌侵染过程中的生物学功能，解析RsNE2对植物不同层次免疫反应的影响，详细阐明其抑制免疫基因表达的分子机制，并探讨通过编辑TGAs的互作位点提高植物抗青枯病的可能。项目的完成将揭示植物免疫基因表达被病原细菌抑制的新机理，扩展对效应蛋白干涉植物先天免疫的认知，为植物抗青枯病的改良育种提供新策略和理论支撑。

Bacterial wilt caused by Ralstonia solanacearum is a kind of devastating vascular disease with global geographic distribution, extreme aggressiveness and hosts diversity, which lacks effective prevention methods and stable broad disease resistant gene resources. Plants rely on the innate immune to count microbe infection, while R. solanacearum could suppress plant immune response with the type III secreted system related effectors. However, how these proteins interfere with the expression of plant immune genes is still elusive. In previous studies, we found that the plant nuclear-localized effector RsNE2 of R. solanacearum significantly inhibits the expression of immune-related genes, and interacts with TGAs, a group of key transcription factors in plant defense. These results suggest that a novel mechanism of phytobacteria hijacks plant transcription factors to inhibit the immune response. This project aims to dissect the biological functions of RsNE2 in the process of R. solanacearum infection, and the effect of RsNE2 on different layers of plant immunity. We will elucidate how RsNE2 inhibits the function of TGA transcription factors which interfere with the induction of plant immune genes, and explore the possibility of generating bacterial wilt-resistant plant materials by editing TGAs interaction sites. The completion of the project will reveal the new mechanism of plant immune-related gene expression is inhibited by phytobacteria, extend the knowledge of the bacterial effectors subvert plant innate immunity, and provide a new strategy for breeding of bacterial wilt resistance crop.