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Type II toxin-antitoxin system, RatAB, contributes to oxidative resistance, biofilm formation and virulence of Edwardsiella piscicida

文献类型： 外文期刊

作者： Du, Chunmei 1 ; Zhang, Wanlin 1 ; Gu, Hanjie 2 ; Dong, Xiwen 1 ; Hu, Yonghua 2 ;

作者机构： 1.Jiamusi Univ, Coll Life Sci, Jiamusi 154007, Peoples R China

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

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

4.Hainan Prov Key Lab Funct Components Res & Utiliz, Haikou, Hainan, Peoples R China

关键词： Edwardsiella piscicida; pathogenicity; RatAB; stress resistance; type II Toxin-antitoxin

期刊名称：AQUACULTURE RESEARCH （ 影响因子：2.184； 五年影响因子：2.447 ）

ISSN： 1355-557X

年卷期： 2022 年 53 卷 7 期

页码：

收录情况： SCI

摘要： Since the diversity and importance of its role, the type II TA system is attracting increasing attention from researchers. Edwardsiella piscicida is becoming a leading pathogen that threatens seawater and fresh aquaculture, and has been supposed to be a model organism for the study of intracellular infections. Currently, the pathogenesis of E. piscicida remains unclear, and some new pathogenic factors need to be identified. Type II TA system is largely unknown in E. piscicida. In this study, a type II TA system, RatAB, was identified and characterized in E. piscicida. RatA shares high sequence homology with RatA family toxin, and RatB shares high sequence homology with RnfH family protein. ratA and ratB form a bicistronic operon. The biological roles of RatAB were studied by mutants TX01 Delta ratA and TX01 Delta ratAB, and corresponding complementary strains. The growths of TX01 Delta ratA and TX01 Delta ratAB were similar to that of TX01 in normal LB medium. However, TX01 Delta ratA, especially TX01 Delta ratAB, were more sensitive to oxidation pressure than wild strain TX01. Two mutants' abilities to form persistent bacteria were markedly reduced compared with TX01. The deletions of ratA and ratAB reduced bacterial biofilm formation. Cell infection test indicated that the ratA and ratAB mutations damaged E. piscicida ' s ability to adhere and invade host non-phagocyte and weaken the ability of bacterial to survive and reproduce in host phagocyte. Consistently, in vivo infection tests confirmed that ratA and ratAB were required for bacterial dissemination in host tissues. Taken together, our findings demonstrate for the first time that RatAB is requisite for resistance to adversity and full virulence of E. piscicida.

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