A σ^E-Mediated Temperature Gauge Controls a Switch from LuxR-Mediated Virulence Gene Expression to Thermal Stress Adaptation in <i>Vibrio alginolyticus</i>

Abstract

<div><p>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 σ^E, an alternative sigma factor, during the control of virulence-related gene expression and adaptations to temperature elevations in the zoonotic pathogen <i>Vibrio alginolyticus</i>. An <i>rpoE</i> null <i>V</i>. <i>alginolyticus</i> mutant was unable to adapt to various stresses and was survival-deficient in fish. In wild type <i>V</i>. <i>alginolyticus</i>, the expression of LuxR-regulated virulence factors increased as the temperature was increased from 22°C to 37°C, but mutants lacking σ^E did not respond to temperature, indicating that σ^E is critical for the temperature-dependent upregulation of virulence genes. Further analyses revealed that σ^E binds directly to -10 and -35 elements in the <i>luxR</i> promoter that drive its transcription. ChIP assays showed that σ^E binds to the promoter regions of <i>luxR</i>, <i>rpoH</i> and <i>rpoE</i> at high temperatures (e.g., 30°C and 37°C). However, at higher temperatures (42°C) that induce thermal stress, σ^E binding to the <i>luxR</i> promoter decreased, while its binding to the <i>rpoH</i> and <i>rpoE</i> promoters was unchanged. Thus, the temperature-dependent binding of σ^E to distinct promoters appears to underlie a σ^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.</p></div