A temperature-responsive regulator that enhances virulence in the kiwifruit canker pathogen Pseudomonas syringae pv. actinidiae

文献类型： 外文期刊

第一作者： He, Xueting

作者： He, Xueting;Zhang, Yifei;Xu, Chenbei;Fu, Kaidi;Zhang, Tiantian;Chen, Tingtao;Murero, Aprodisia;Shao, Xiaolong;Qian, Guoliang;Ding, Yiqing;Ding, Yiqing;Ding, Yiqing;Xu, Yuan;Chen, Cheng;Li, Li;Zhong, Caihong;Huang, Lili;Deng, Xin;Deng, Xin

作者机构：

关键词： Kiwifruit canker disease; Pseudomonas syringae pv. actinidae; Low temperature; Heat shock protein; HrpL; Type III secretion system

期刊名称：COMPUTATIONAL AND STRUCTURAL BIOTECHNOLOGY JOURNAL （ 影响因子：4.1； 五年影响因子：5.2 ）

ISSN： 2001-0370

年卷期： 2025 年 27 卷

页码：

收录情况： SCI

摘要： Pseudomonas syringae pv. actinidiae (Psa), the causative agent of kiwifruit canker disease, poses significant threats to global kiwifruit production, resulting in substantial economic losses. Disease incidence is notably higher under cooler temperatures (<20 degrees C), yet the molecular mechanisms underlying Psa's temperature-dependent virulence remain poorly understood. Here, we identify RS16350, encoding a heat shock protein homolog, as a positive regulator of Psa pathogenicity specifically at low temperature (16 degrees C) but not at optimal growth temperature (28 degrees C). Mechanistic studies reveal that RS16350 physically interacts with HrpL, the RpoN-dependent sigma factor controlling type III secretion system (T3SS) expression in Psa. This interaction enhances HrpL's binding affinity to the hrp-box promoter element, thereby upregulating T3SS effector genes and increasing virulence. We designate this novel regulator as TrpR2 (temperature-responsive pathogenic regulator 2). These findings provide molecular insights into temperature-modulated virulence in a key plant pathogen and identify potential targets for developing innovative disease control strategies.

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