文献类型：期刊文献

英文题名：Fur-mediated regulation of hydrogen sulfide synthesis, stress response, and virulence in Edwardsiella piscicida

作者：Zhang, Riyu[1];Bu, Yifan[1];Zhang, Yuanxing[2,3];Choi, Sang Ho[4];Wang, Qiyao[1,5,6];Ma, Yue[1,3,5];Shao, Shuai[1,3,5]

机构：[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]Southern Marine Sci & Engn Guangdong Lab Zhuhai, Zhuhai 519000, Peoples R China;[3]Shanghai Engn Res Ctr Maricultured Anim Vaccines, Shanghai, Peoples R China;[4]Seoul Natl Univ, Dept Agr Biotechnol, Natl Res Lab Mol Microbiol & Toxicol, Seoul, South Korea;[5]Lab Aquat Anim Dis MOA, Shanghai, Peoples R China;[6]Shanghai Haosi Marine Biotechnol Co Ltd, Shanghai, Peoples R China

年份：2024

卷号：284

外文期刊名：MICROBIOLOGICAL RESEARCH

收录：;EI(收录号：20241816002766);WOS:【SCI-EXPANDED(收录号:WOS:001235059000001)】；

基金：This work was supported by grants from the National Key Research and Development Program (2022YFE0101200) , the Shanghai Municipal Science and Technology Commission Technical Leader Project (21XD1431900) , and the China Agriculture Research System of MOF and MARA (CARS -47) .

语种：英文

外文关键词：Edwardsiella piscicida; fur; Hydrogen sulfide; in vivo colonization

摘要：The production of endogenous hydrogen sulfide (H2S) is an important phenotype of bacteria. H2S plays an important role in bacterial resistance to ROS and antibiotics, which significantly contributes to bacterial pathogenicity. Edwardsiella piscicida, the Gram -negative pathogen causing fish edwardsiellosis, has been documented to produce hydrogen sulfide. In the study, we revealed that Ferric uptake regulator (Fur) controlled H2S synthesis by activating the expression of phsABC operon. Besides, Fur participated in the bacterial defense against ROS and cationic antimicrobial peptides and modulated T3SS expression. Furthermore, the disruption of fur exhibited a significant in vivo colonization defect. Collectively, our study demonstrated the regulation of Fur in H2S synthesis, stress response, and virulence, providing a new perspective for better understanding the pathogenesis of Edwardsiella.