文献类型：期刊文献

英文题名：A σE-Mediated Temperature Gauge Controls a Switch from LuxR-Mediated Virulence Gene Expression to Thermal Stress Adaptation in Vibrio alginolyticus

作者：Gu, Dan[1];Guo, Min[1];Yang, Minjun[2];Zhang, Yuanxing[1,3,4];Zhou, Xiaohui[5];Wang, Qiyao[1,3,4]

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]Shanghai Collaborat Innovat Ctr Biomfg Technol, Shanghai, Peoples R China;[4]Shanghai Engn Res Ctr Maricultured Anim Vaccines, Shanghai, Peoples R China;[5]Univ Connecticut, Dept Pathobiol & Vet Sci, Storrs, CT 06269 USA

年份：2016

卷号：12

期号：6

外文期刊名：PLOS PATHOGENS

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000379345300017)】；

基金：This work was supported by grants from the National Natural Science Foundation of China (www.nsfc.gov.cn) (Nos. 31372560 and 41376128) to QW and YZ, respectively, the Shanghai Youth Sailing Program (www.stcsm.gov.cn) (No. 14YF1413700) to MY, and the National Institute of Food and Agriculture, US Department of Agriculture Grant (CONS00935) to XZ. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

语种：英文

摘要：In vibrios, the expression of virulence factors is often controlled by LuxR, the master quorum-sensing regulator. Here, we investigate the interplay between LuxR and sigma(E), an alternative sigma factor, during the control of virulence-related gene expression and adaptations to temperature elevations in the zoonotic pathogen Vibrio alginolyticus. An rpoE null V. alginolyticus mutant was unable to adapt to various stresses and was survival-deficient in fish. In wild type V. alginolyticus, the expression of LuxR-regulated virulence factors increased as the temperature was increased from 22 degrees C to 37 degrees C, but mutants lacking sigma(E) did not respond to temperature, indicating that sigma(E) is critical for the temperature-dependent upregulation of virulence genes. Further analyses revealed that sigma(E) binds directly to -10 and -35 elements in the luxR promoter that drive its transcription. ChIP assays showed that sigma(E) binds to the promoter regions of luxR, rpoH and rpoE at high temperatures (e.g., 30 degrees C and 37 degrees C). However, at higher temperatures (42 degrees C) that induce thermal stress, sigma(E) binding to the luxR promoter decreased, while its binding to the rpoH and rpoE promoters was unchanged. Thus, the temperature-dependent binding of sigma(E) to distinct promoters appears to underlie a sigma(E)-controlled switch between the expression of virulence genes and adaptation to thermal stress. This study illustrates how a conserved temperature response mechanism integrates into quorum-sensing circuits to regulate both virulence and stress adaptation.