| 猕猴桃溃疡病菌不致病菌株G230的鉴定及形成原因分析 |
| 点此下载全文 |
| 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.植物保护学报,2023,50(4):932-944 |
| DOI：10.13802/j.cnki.zwbhxb.2023.2022005 |
| 摘要点击次数: |
| 全文下载次数: |
|
|
| 中文摘要: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。 |
| 中文关键词:猕猴桃溃疡病 致病性 转座子 III型分泌系统 hrpS基因 |
| |
| Determining the molecular basis for the loss-of-virulence in bacterial pathogen Pseudomonas syringae pv. actinidiae isolate G230 |
| Author Name | Affiliation | E-mail | | Xie Ting | College of Agriculture, Guizhou University, Guiyang 550025, Guizhou Province, China | | | Wu Shiping | Institute of Plant Protection, Guizhou Academy of Agricultural Sciences, Guiyang 550006, Guizhou Province, China | | | Zhang Qinghua | College of Agriculture, Guizhou University, Guiyang 550025, Guizhou Province, China | | | Wang Ziying | College of Agriculture, Guizhou University, Guiyang 550025, Guizhou Province, China | | | Mo Xiangkai | College of Agriculture, Guizhou University, Guiyang 550025, Guizhou Province, China | | | Yang Zaifu | College of Agriculture, Guizhou University, Guiyang 550025, Guizhou Province, China | | | Zhao Zhibo | College of Agriculture, Guizhou University, Guiyang 550025, Guizhou Province, China | zbzhao@gzu.edu.cn | | Huang Lili | College of Plant Protection, Northwest A&F University, Yangling 712100, Shaanxi Province, China | huanglili@nwsuaf.edu.cn |
|
|
| 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. |
| keywords:bacterial canker of kiwifruit pathogenicity transposon T3SS hrpS gene |
| 查看全文 查看/发表评论 下载PDF阅读器 |
|
|
|
|
您是本站第 14348373 版权所有：植物保护学报 京ICP备05006550号-2 主管单位：中国科协 主办单位：中国植物保护学会、中国农业大学 地址：北京市圆明园西路2号 中国农业大学植物保护学院 植物保护学报编辑部 电话：010-62732528 电子邮件：zbxb@cau.edu.cn 技术支持： 北京勤云科技发展有限公司 |
