Abstract
Vibrio cholerae is the causative agent of the devastating diarrheal disease cholera. A number of regulatory pathways are involved in V. cholerae pathogenesis and antibiotic resistance. For example, there are over 40 LysR-family proteins in the V. cholerae genome, but most of their functions are unknown. In this study, we examine the role of VC2323 (TehAVc) and its divergently transcribed LysR-family regulator VC2324 (TehRVc) in V. cholerae pathogenesis. We found that in V. cholerae C6706, the expression of tehAVc is dependent on TehRVc. VC2323 (TehAVc), homologous to the Escherichia coli tellurite resistance protein (TehAEc), differs from TehAEc in that TehAVc has no noticeable role in tellurite resistance but instead contributes to chloramphenicol resistance. Interestingly, both tehAVc and tehRVc mutants were defective in colonization of infant mice. Though the expression of a key virulence gene tcpA was not affected in either of these mutants, tehAVc mutants failed to attach to mouse intestinal surfaces in the presence of crude bile, suggesting a new role of the TehAVc-TehRVc pair in V. cholerae pathogenesis.
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