文献类型： 外文期刊

作者： He, Xueting ¹ ; Zhang, Yifei ¹ ; Xu, Chenbei ¹ ; Fu, Kaidi ¹ ; Ding, Yiqing ² ; Zhang, Tiantian ¹ ; Chen, Tingtao ¹ ; Murero, Aprodisia ¹ ; Wang, Limin ¹ ; Xu, Yuan ⁵ ; Chen, Cheng ⁵ ; Yang, Jinghui ¹ ; Li, Li ⁶ ; Zhong, Caihong ⁶ ; Huang, Lili ⁷ ; Deng, Xin ⁸ ; Shao, Xiaolong ¹ ; Qian, Guoliang ¹ ;

作者机构： 1.Nanjing Agr Univ, Coll Plant Protect, State Key Lab Agr & Forestry Biosecur, Nanjing 210095, Peoples R China

2.Guangdong Acad Agr Sci, Inst Fruit Tree Res, Guangzhou 510640, Peoples R China

3.Minist Agr & Rural Affairs, Key Lab South Subtrop Fruit Biol & Genet Resource, Guangzhou 510640, Peoples R China

4.Guangdong Prov Key Lab Sci & Technol Res Fruit Tre, Guangzhou 510640, Peoples R China

5.Jiangsu Acad Agr Sci, Jiangsu Hilly Area Zhenjiang Inst Agr Sci, Jurong 212400, Peoples R China

6.Chinese Acad Sci, CAS Engn Lab Kiwifruit Ind Technol, CAS Key Lab Plant Germplasm Enhancement & Specialt, Wuhan Bot Garden, Wuhan 430074, Hubei, Peoples R China

7.Northwest A&F Univ, Coll Plant Protect, State Key Lab Crop Stress Biol Arid Areas, Yangling 712100, Shaanxi, Peoples R China

8.City Univ Hong Kong, Dept Biomed Sci, Kowloon Tong, Hong Kong, Peoples R China

9.City Univ Hong Kong, Shenzhen Res Inst, Shenzhen 518057, Guangdong, Peoples R China

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.