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

PLoS Pathogens

Xiaohui Zhou¹  Qiyao Wang²  Minjun Yang³  Min Guo⁴  Yuanxing Zhang⁴  Dan Gu⁴ 

[1] Shanghai Collaborative Innovation Center for Biomanufacturing Technology, Shanghai, China;Shanghai Engineering Research Center of Maricultured Animal Vaccines, Shanghai, China;Shanghai—MOST Key Laboratory of Health and Disease Genomics, Chinese National Human Genome Center at Shanghai, Shanghai, China;State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai, China

关键词: Virulence factors;    Vibrio;    Promoter regions;    Gene expression;    Electrophoretic mobility shift assay;    Thermal stresses;    Stress signaling cascade;    Polymerase chain reaction;   

DOI  :  10.1371/journal.ppat.1005645

学科分类：生物科学（综合）

来源: Public Library of Science

【 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 σE, 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°C to 37°C, but mutants lacking σE did not respond to temperature, indicating that σE is critical for the temperature-dependent upregulation of virulence genes. Further analyses revealed that σE binds directly to -10 and -35 elements in the luxR promoter that drive its transcription. ChIP assays showed that σE binds to the promoter regions of luxR, rpoH and rpoE at high temperatures (e.g., 30°C and 37°C). However, at higher temperatures (42°C) that induce thermal stress, σE binding to the luxR promoter decreased, while its binding to the rpoH and rpoE promoters was unchanged. Thus, the temperature-dependent binding of σE to distinct promoters appears to underlie a σE-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.

【 授权许可】

CC BY