Small RNA coaR contributes to intestinal colonization in Vibrio cholerae via the two‐component system EnvZ/OmpR. (5th January 2020)

• Record Type: Journal Article
• Authors: Xi, Daoyi; Li, Yujia; Yan, Junxiang; Li, Yuehua; Wang, Xiaochen; Cao, Boyang
• Other Names: Oliver James D. guestEditor.; Destoumieux‐Garzon Delphine guestEditor.; Pruzzo Carla guestEditor.; Baker‐Austin Craig guestEditor.
• Is Part Of: Environmental microbiology. Volume 22:Number 10(2020)
• Page Start: 4231
• Page End: 4243
• Publication Date: 2020-01-05
• Subjects: Microbial ecology -- Periodicals; Environmental Microbiology -- Periodicals; 579.17
• DOI: 10.1111/1462-2920.14906
• Languages: English
• ISSNs: 1462-2912

Abstract

Summary: Vibrio cholerae is a waterborne bacterium responsible for worldwide outbreaks of acute and fatal cholera. Recently, small regulatory RNAs (sRNAs) have become increasingly recognized as important regulators of virulence gene expression in response to environmental signals. In this study, we determined that two‐component system EnvZ/OmpR was required for intestinal colonization in V. cholerae O1 EI Tor strain E12382. Analysis of the characteristics of OmpR revealed a potential binding site in the intergenic region between vc1470 and vc1471, and qRT‐PCR showed that expression of the intergenic region increased 5.3‐fold in the small intestine compared to LB medium. Race and northern blot assays were performed and demonstrated a new sRNA, coaR (cholerae osmolarity and acidity related regulatory RNA). A Δ coaR mutant showed a deficient colonization ability in small intestine with CI of 0.15. We identified a target of coaR, tcpI, a negative regulator of the major pilin subunit of TcpA. The Δ tcpI mutant has an increased colonization with CI of 3.16. The expression of coaR increased 2.8‐fold and 3.3‐fold under relative acidic and hypertonic condition. In summary, coaR was induced under the condition of high osmolarity and acid stress via EnvZ/OmpR and explained that tcpI relieves pH‐mediated repression of toxin co‐regulated pilus synthesis.