| 猕猴桃溃疡病菌不致病菌株G230的鉴定及形成原因分析 |
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| 引用本文： | 谢婷,吴石平,张清华,王紫颖,莫祥恺,杨再福,赵志博,黄丽丽.猕猴桃溃疡病菌不致病菌株G230的鉴定及形成原因分析[J].植物保护学报,2023,50(4):932-944. |
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| 作者姓名： | 谢婷 吴石平 张清华 王紫颖 莫祥恺 杨再福 赵志博 黄丽丽 |
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| 作者单位： | 贵州大学农学院, 贵阳 550025;贵州省农业科学院植物保护研究所, 贵阳 550006;西北农林科技大学植物保护学院, 杨凌 712100 |
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| 基金项目： | 国家自然科学基金（31860486），贵州省科技支撑项目（黔科合支撑[2020]1Y131号） |
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| 摘 要： | 为探索田间猕猴桃溃疡病菌Pseudomonas syringae pv. actinidiae(Psa)致病力丧失的分子机制，针对从猕猴桃果园中分离获得的1株不致病菌株G230，通过特异性引物检测和多基因序列分析明确其分类地位，并设计引物检测其是否由已知遗传变异引起，通过比较基因组学、基因表达、超敏反应和荧光素酶报告菌株检测确定引起菌株G230致病力丧失的原因。结果表明，不致病菌株G230为Psa生物型3(Psa3)，其致病缺陷不是由已报道的遗传变异引起；基于基因组比较分析发现菌株G230中的hrpS基因被转座子ISPsy36插入破坏，导致Ⅲ型分泌系统（type Ⅲ secretion system,T3SS）不能正常表达；而在不致病菌株G230中表达hrpS基因后能恢复其T3SS功能，使其具备致病能力及激发非寄主超敏反应的能力。表明转座子ISPsy36插入hrpS基因内部可以破坏Psa的T3SS功能进而使其丧失致病力，这是自然条件下Psa3丧失致病力的一种新型机制。
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| 关 键 词： | 猕猴桃溃疡病 致病性 转座子 Ⅲ型分泌系统 hrpS基因 |
| 收稿时间： | 2022/1/1 0:00:00 |
Determining the molecular basis for the loss-of-virulence in bacterial pathogen Pseudomonas syringae pv. actinidiae isolate G230 |
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| Xie Ting,Wu Shiping,Zhang Qinghu,Wang Ziying,Mo Xiangkai,Yang Zaifu,Zhao Zhibo,Huang Lili.Determining the molecular basis for the loss-of-virulence in bacterial pathogen Pseudomonas syringae pv. actinidiae isolate G230[J].Acta Phytophylacica Sinica,2023,50(4):932-944. |
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| Authors: | Xie Ting Wu Shiping Zhang Qinghu Wang Ziying Mo Xiangkai Yang Zaifu Zhao Zhibo Huang Lili |
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| Institution: | College of Agriculture, Guizhou University, Guiyang 550025, Guizhou Province, China;Institute of Plant Protection, Guizhou Academy of Agricultural Sciences, Guiyang 550006, Guizhou Province, China; College of Plant Protection, Northwest A&F University, Yangling 712100, Shaanxi Province, China |
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| Abstract: | To gain insight into the molecular basis underlying spontaneous loss-of-virulence in natural populations of Pseudomonas syringae pv. actinidiae (Psa), the causative agent of kiwifruit bacterial canker, a non-pathogenic isolate G230 from a kiwifruit orchard was identified using Psa-specific PCR detection and multi-locus sequence analysis, and the genetic cause of the non-pathogenic phenotype was determined with PCR detection of several known transposon-insertion events, comparative genomics and gene expression methods, followed by the detection of type III secretion system (T3SS) via a nanoluciferase reporter system and the hypersensitive response (HR) indicator on the non-host Nicotiana benthamiana leaves. The non-pathogenic isolate G230 was identified as Psa biovar 3 (Psa3), and results revealed that its loss of virulence was not caused by known transposon-insertion events in Psa3. Moreover, a novel transposon-insertion event inside hrpS gene by ISPsy36 was found in G230, and after expression of the hrpS gene in non-pathogenic isolate G230 resulted in a functional T3SS, which was necessary for pathogenicity in Psa3 and HR induction in non-host plants. Taken together, the insertion of ISPsy36 into the hrpS gene, which results in T3SS deficiency in the non-pathogenic isolate G230, represents a novel mode of action underlying spontaneous loss-of-virulence in natural populations of Psa3. |
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| Keywords: | bacterial canker of kiwifruit pathogenicity transposon T3SS hrpS gene |
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