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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  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 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  luxR  promoter that drive its transcription. ChIP assays showed that σ E  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, σ E  binding to the  luxR  promoter decreased, while its binding to the  rpoH  and  rpoE  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.

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