文献类型：期刊文献

英文题名：Long-chain unsaturated fatty acids sensor controlling the type III/VI secretion system is essential for Edwardsiella piscicida infection

作者：Xia, Feng[1];Liu, Yihan[1];Wei, Lifan[1];Shao, Shuai[1,2,3];Zhang, Yuanxing[2,3];Ma, Yue[1,2,3];Wang, Qiyao[1,2,3,4]

机构：[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]Shanghai Engn Res Ctr Maricultured Anim Vaccines, Shanghai, Peoples R China;[3]Lab Aquat Anim Dis MOA, Shanghai 200237, Peoples R China;[4]Shanghai Haosi Marine Biotechnol Co Ltd, Shanghai, Peoples R China

年份：2024

卷号：285

外文期刊名：MICROBIOLOGICAL RESEARCH

收录：;EI(收录号：20242116134264);WOS:【SCI-EXPANDED(收录号:WOS:001244331200001)】；

基金：This work was supported by grants from the National Natural Science Foundation of China (32130108) , 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; EsrC; Fish pathogen; T3SS; T6SS; Unsaturated fatty acids UFA

摘要：Edwardsiella piscicida is an acute marine pathogen that causes severe damage to the aquaculture industry worldwide. The pathogenesis of E. piscicida is dependent mainly on the type III secretion system (T3SS) and type VI secretion system (T6SS), both of which are critically regulated by EsrB and EsrC. In this study, we revealed that fatty acids influence T3SS expression. Unsaturated fatty acids (UFAs), but not saturated fatty acids (SFAs), directly interact with EsrC, which abolishes the function of EsrC and results in the turn-off of T3/T6SS. Moreover, during the in vivo colonization of E. piscicida, host fatty acids were observed to be transported into E. piscicida through FadL and to modulate the expression of T3/T6SS. Furthermore, the esrCR38G mutant blocked the interaction between EsrC and UFAs, leading to dramatic growth defects in DMEM and impaired colonization in HeLa cells and zebrafish. In conclusion, this study revealed that the interaction between UFAs and EsrC to turn off T3/T6SS expression is essential for E. piscicida infection.