Vibrio cholerae VC1741 (PsrA) enhances the colonization of the pathogen in infant mice intestines in the presence of the long-chain fatty acid, oleic acid.

Vibrio cholerae is a natural inhabitant of aquatic environments and causes the epidemic diarrheal disease known as cholera. Fatty acid metabolism is closely related to the pathogenicity of V. cholerae. The TetR family transcriptional repressor PsrA regulates the β-oxidation pathway in Pseudomonas aeruginosa; however, little is known about its regulation in V. cholerae. In this study, qRT-PCR revealed that the expression of vc1741 (psrA) increased 40-fold in the small intestines of infant mice compared with that grown in LB medium. The Δvc1741 mutant showed a significant defected in the ability to colonize the small intestines of infant mice with a competitive index (CI) of 0.53. EMSAs indicated that VC1741 could directly bind to the promoter regions of vc1741-fadE1, fadBA, and fadIJ operons, and these bindings were reversed upon addition of the long-chain fatty acid (LCFA), oleic acid. The expression levels of the fadB, fadA, fadI, and fadJ genes were all elevated by approximately 2-fold in the Δvc1741 mutant strain compared with that in the wild-type strain in LB medium, indicating that VC1741 is a repressor for these genes involved in fatty acid degradation. Moreover, ΔfadBA, ΔfadB, and ΔfadA isogenic mutants showed defective abilities to colonize the small intestines of infant mice, with CI values of 0.64, 0.73, and 0.74, respectively. These data provided a mechanistic model in which LCFAs affect the expression of VC1741 to control fatty acid degradation and virulence in V. cholerae.