文献类型：期刊文献

英文题名：Transcriptomic dissection of the horizontally acquired response regulator EsrB reveals its global regulatory roles in the physiological adaptation and activation of T3SS and the cognate effector repertoire in Edwardsiella piscicida during infection toward turbot

作者：Liu, Yang[1];Zhao, Luyao[1];Yang, Minjun[2];Yin, Kaiyu[1];Zhou, Xiaohui[3];Leung, Ka Yin[1,4];Liu, Qin[1,5,6];Zhang, Yuanxing[1,5,6];Wang, Qiyao[1,5,6]

机构：[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai, Peoples R China;[2]Chinese Natl Human Genome Ctr Shanghai, Shanghai MOST Key Lab Hlth & Dis Genom, Shanghai, Peoples R China;[3]Univ Connecticut, Dept Pathobiol & Vet Sci, Storrs, CT USA;[4]Trinity Western Univ, Dept Biol, Fac Nat & Appl Sci, Langley, BC, Canada;[5]Shanghai Engn Res Ctr Maricultured Anim Vaccines, Shanghai, Peoples R China;[6]Shanghai Collaborat Innovat Ctr Biomfg Technol, Shanghai, Peoples R China

年份：2017

卷号：8

期号：7

起止页码：1355

外文期刊名：VIRULENCE

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000416969700039)】；

基金：This work was supported by National Natural Science Foundation of China under grant number 31430090 and 31400122; the Ministry of Agriculture of China under grant number CARS-50 and nyhyzx-201303047; and the Shanghai Pujiang Program under grant number 16PJD018. K.Y.L was supported by Natural Sciences and Engineering Research Council of Canada (NSERC) Discovery Grant (372373-2010) and X.H.Z was supported by NIH R01AI118943

语种：英文

外文关键词：Edwardsiella piscicida; effectors; EsrB; RNA-seq; T3SS; T6SS

摘要：Edwardsiella piscicida is the leading pathogen threatening worldwide aquaculture industries. The 2-component system (TCS) EsrA-EsrB is essential for the pathogenesis of this bacterium. However, little is known about the regulon and regulatory mechanism of EsrA-EsrB or about the factors that mediate the interaction of TCS with bacterial hosts. Here, our RNA-seq analysis indicated that EsrB strongly induces type III and type VI secretion systems (T3/T6SS) expression and that it modulates the expression of both physiology- and virulence-associated genes in E. piscicida grown in DMEM. EsrB binds directly to a highly conserved 18-bp DNA motif to regulate the expression of T3SS and other genes. EsrB/DMEM-activated genes include 3 known and 6 novel T3SS-dependent effectors. All these effector genes are highly induced by EsrB during the late stage of in vivo infection in fish. Furthermore, although in vivo colonization by the bacterium relies on EsrB and T3/T6SS expression, it does not require the expression of individual effectors other than EseJ. The mutant lacking these 9 effectors showed significant defects in in vivo colonization and virulence toward turbot, and, more importantly, a high level of protection against challenges by wild-type E. piscicida, suggesting that it may represent a promising live attenuated vaccine. Taken together, our data demonstrate that EsrB plays a global regulatory role in controlling physiologic responses and the expression of T3SS and its cognate effector genes. Our findings will facilitate further work on the mechanism of molecular pathogenesis of this bacterium during infection.