文献类型：期刊文献

英文题名：FabR senses long-chain unsaturated fatty acids to control virulence in pathogen Edwardsiella piscicida

作者：Shao, Shuai[1];Zhang, Yi[1];Yin, Kaiyu[1];Zhang, Yuanxing[2,3];Wei, Lifan[1,4];Wang, Qiyao[1,3]

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, Peoples R China;[3]Shanghai Engn Res Ctr Maricultured Anim Vaccines, Shanghai, Peoples R China;[4]Shanghai Jiao Tong Univ, Peoples Hosp 9, Coll Stomatol, Sch Med,Dept Endodont & Operat Dent, Shanghai, Peoples R China

年份：2022

卷号：117

期号：4

起止页码：737

外文期刊名：MOLECULAR MICROBIOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000740266500001)】；

基金：National Natural Science Foundation of China, Grant/Award Number: 32002436 and 32130108; Science and Technology Commission of Shanghai Municipality, Grant/Award Number: 21XD1431900; Fundamental Research Funds for the Central Universities, Grant/Award Number: 222201211716; China Agriculture Research System of MOF and MARA, Grant/Award Number: CARS-47; China Postdoctoral Science Foundation, Grant/Award Number: 2020M671034

语种：英文

外文关键词：Edwardsiella piscicida; EsrB; FabR; fatty acid; T3SS

摘要：Long-chain unsaturated fatty acids (UFAs) can serve as nutrient sources or building blocks for bacterial membranes. However, little is known about how UFAs may be incorporated into the virulence programs of pathogens. A previous investigation identified FabR as a positive regulator of virulence gene expression in Edwardsiella piscicida. Here, chromatin immunoprecipitation-sequencing coupled with RNA-seq analyses revealed that 10 genes were under the direct control of FabR, including fabA, fabB, and cfa, which modulate the composition of UFAs. The binding of FabR to its target DNA was facilitated by oleoyl-CoA and inhibited by stearoyl-CoA. In addition, analyses of enzyme mobility shift assay and DNase I footprinting with wild-type and a null mutant (F131A) of FabR demonstrated crucial roles of FabR in binding to the promoters of fabA, fabB, and cfa. Moreover, FabR also binds to the promoter region of the virulence regulator esrB for its activation, facilitating the expression of the type III secretion system (T3SS) in response to UFAs. Furthermore, FabR coordinated with RpoS to modulate the expression of T3SS. Collectively, our results elucidate the molecular machinery of FabR regulating bacterial fatty acid composition and virulence in enteric pathogens, further expanding our knowledge of its crucial role in host-pathogen interactions.