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Small RNA sR158 Participates in Oxidation Stress Tolerance and Pathogenicity of Edwardaiella piscicida by Regulating TA System YefM-YoeB

文献类型： 外文期刊

作者： Dong, Jinggang 1 ; Gu, Hanjie 2 ; Huang, Huiqin 2 ; Tang, Xiaoqian 1 ; Hu, Yonghua 2 ;

作者机构： 1.Ocean Univ China, Lab Pathol & Immunol Aquat Anim, KLMME, Qingdao 266071, Peoples R China

2.Hainan Inst Trop Agr Resources, Inst Trop Biosci & Biotechnol, CATAS, Haikou 571101, Peoples R China

3.Hainan Inst Trop Agr Resources, Key Lab Biol & Genet Resources Trop Crops Hainan P, Haikou 571101, Peoples R China

4.CATAS, Zhanjiang Expt Stn, Zhanjiang 524013, Peoples R China

5.Hainan Prov Key Lab Funct Components Res & Utiliza, Haikou 571101, Peoples R China

6.Pilot Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao 266071, Peoples R China

期刊名称：AQUACULTURE RESEARCH （ 影响因子：2.0； 五年影响因子：2.3 ）

ISSN： 1355-557X

年卷期： 2023 年 2023 卷

页码：

收录情况： SCI

摘要： In recent years, the role of bacterial sRNAs in adversity tolerance and pathogens has attracted increasing attention. A great number of virulence-related sRNAs were reported in a variety of human pathogens. However, only a few sRNAs from aquatic pathogens were reported. In our previous study, a novel sRNA, sR158, was identified in Edwardsiella piscicida, an important aquatic pathogen, but its function remains unknown. In the same aquatic pathogen, we also identified a type II TA system, YefM-YoeB, in another study. In the current report, we found that the expression of yefM-yoeB in E. piscicida was regulated by sR158, which is dependent on the RNA chaperon Hfq. The deletion of sR158 reduced bacterial tolerance to oxidation pressure, enhanced bacterial capacity for biofilm formation, increased bacterial adhesion and invasion of host cells and immune tissues, and boosted bacterial general virulence, which are consistent with the effects caused by the deletion of YefM-YoeB. These findings indicate that sR158 participates in the stress resistance and virulence of E. piscicida by regulating YefM-YoeB. Our result is the first report that the type II TA system is regulated by sRNA, which provides new insights into the regulatory role of bacterial sRNA.

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