Ralstonia solanacearum injected protein RipH1 targets transcription factor B-box (BBX)-containing protein 31 in Arabidopsis thaliana to manipulate plant immunity

文献类型： 外文期刊

第一作者： Ju, Lili

作者： Ju, Lili;Yang, Shanshan;Liang, Xiaoyan;Zhang, Zhiheng;Wang, Hao;Qin, Tong;Li, Fayu;Huang, Jingjing;Chen, Dong;Zheng, Dehong;Wang, Peng;He, Yongqiang;Yu, Wenjin;Zhang, Xiaoxiao;Zhao, Jianlong

作者机构：

关键词： Type III effector RipH1; AtBBX31; Plant immunity

期刊名称：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES （ 影响因子：8.5； 五年影响因子：8.7 ）

ISSN： 0141-8130

年卷期： 2025 年 318 卷

页码：

收录情况： SCI

摘要： The type III effector RipH1, a conserved virulence factor in Ralstonia solanacearum, manipulates plant immunity by targeting the transcription factor B-box (BBX)-containing protein 31, AtBBX31 in Arabidopsis thaliana. Here, we demonstrate that RipH1 suppresses reactive oxygen species (ROS) production and triggers programmed cell death (PCD) in multiple plant species, including Nicotiana benthamiana, tomato, and Arabidopsis thaliana. Notably, RipH1 negatively regulates the pathogenicity of R. solanacearum GMI1000 in A. thaliana but not in tomato, suggesting host-specific virulence modulation. Yeast two-hybrid, bimolecular fluorescence complementation, and co-immunoprecipitation assays confirm the direct interaction between RipH1 and AtBBX31. This interaction stabilizes both proteins and promotes AtBBX31 membrane localization, independent of the ubiquitination pathway. Notably, AtBBX31 positively regulates resistance to R. solanacearum and ROS production, and RipH1 disrupts its binding to the promoter of AtBBX29, which positively regulates resistance to R. solanacearum and ROS production. By targeting AtBBX31, RipH1 impairs the immune signaling of the AtBBX31-AtBBX29 axis. This study reveals a novel mechanism by which bacterial effectors hijack plant transcription factors to reprogram immunity pathways. The findings highlight the importance of biological macromolecules in plant-pathogen interactions and provide insights for developing durable resistance strategies against bacterial wilt.

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