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

Date Published: June 2, 2016

Publisher: Public Library of Science

Author(s): Dan Gu, Min Guo, Minjun Yang, Yuanxing Zhang, Xiaohui Zhou, Qiyao Wang, Andreas J Baumler.


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.

Partial Text

It has been established that warming sea surface temperatures (SST) threatens marine ecosystems, including coral species that reside in coral reefs [1,2]. In addition, elevated sea temperatures are associated with mass mortalities in farmed sea animals [3], and these are often associated with infection by vibrios [4,5]. Elevated SST increases the abundance of marine vibrios, including V. coralliilyticus and V. cholerae [6,7]. However, while temperature does appear to play a more direct and distinct role in temperature-related infection scenarios involving opportunistic vibrios [8–11], the mechanisms underlying this process are largely unknown. Furthermore, vibrios have to adapt to different temperatures, e.g., in the natural residence, during infection or at the extreme ocean conditions. The molecular mechanisms to coordinate gene expression in order to adapt to different temperatures have not been precisely elucidated in vibrios.




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