RcsB-dependent regulation of type VI secretion system in porcine extra-intestinal pathogenic Escherichia coli
文献类型： 外文期刊
作者： Hu, Linlin 1 ; Yu, Feifei 1 ; Liu, Manli 2 ; Chen, Jing 3 ; Zong, Bingbing 1 ; Zhang, Yanyan 1 ; Chen, Tumei 1 ; Wang, Ch 1 ;
作者机构： 1.Huazhong Agr Univ, Coll Vet Med, State Key Lab Agr Microbiol, Wuhan 430070, Hubei, Peoples R China
2.Hubei Acad Agr Sci, Hubei Biopesticide Engn Res Ctr, Wuhan 430064, Hubei, Peoples R China
3.Guangzhou Med Univ, Guangzhou 511436, Guangdong, Peoples R China
4.Cooperat Innovat Ctr Sustainable Pig Prod, Key Lab Prevent Vet Med Hubei Prov, Wuhan 430070, Hubei, Peoples R China
关键词： Rcs cascade; Type VI secretion system; Polymyxin B; Oxidative stress; Adaption
期刊名称：GENE （ 影响因子：3.688； 五年影响因子：3.329 ）
ISSN： 0378-1119
年卷期： 2021 年 768 卷
页码：
收录情况： SCI
摘要： Signal transduction system and specialized secretory devices are crucial for bacteria to sense and adequately adapt in adverse environmental conditions. Therefore, it's crucial for microbes to detect and respond to lethal attacks when envelope is perturbed so as to minimize and fix the damage in milieu. We investigated the adaptive response of porcine extra-intestinal pathogenic Escherichia coli PCN033 to polymyxin B challenge. Treatment with polymyxin B led to rapid and robust activation of Rcs system via RcsF, as well as the accumulation of reactive oxygen species. ExPEC T6SS expression was strongly induced by RcsB in Rcs system, resulting in the reduction in the damage to constitute a survival strategy. Finally, we show that T6SS of ExPEC is involved in its pathogenicity in mouse model. Compared with the wild type strain, the deletion of T6SS genes led to a decrease in the organ colonization ability, and the RcsFS2DM3Q mutant that caused Rcs activation had a stronger colonization ability than the wild type strain. In conclusion, Rcs system orchestrates Rcs cascade to trigger antioxidant defense of T6SS, and presents a typical model in which a bacterium reschedule its transcription network via the Rcs phosphorelay pathway in response to membrane perturbations for survival and pathogenesis.
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