Mucosal penetration primes Vibrio cholerae for host colonization by repressing quorum sensing Academic Article uri icon

Overview

MeSH Major

  • Gene Expression Regulation, Bacterial
  • Intestinal Mucosa
  • Quorum Sensing
  • Repressor Proteins
  • Vibrio cholerae

abstract

  • To successfully infect a host and cause the diarrheal disease cholera, Vibrio cholerae must penetrate the intestinal mucosal layer and express virulence genes. Previous studies have demonstrated that the transcriptional regulator HapR, which is part of the quorum sensing network in V. cholerae, represses the expression of virulence genes. Here, we show that hapR expression is also modulated by the regulatory network that governs flagellar assembly. Specifically, FliA, which is the alternative sigma-factor (sigma(28)) that activates late-class flagellin genes in V. cholerae, represses hapR expression. In addition, we show that mucin penetration by V. cholerae is sufficient to break flagella and so cause the secretion of FlgM, the anti-sigma factor that inhibits FliA activity. During initial colonization of host intestinal tissue, hapR expression is repressed because of low cell density. However, full repression of hapR expression does not occur in fliA mutants, which results in attenuated colonization. Our results suggest that V. cholerae uses flagellar machinery to sense particular intestinal signals before colonization and enhance the expression of virulence genes by modulating the output of quorum sensing signaling.

publication date

  • July 15, 2008

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC2474479

Digital Object Identifier (DOI)

  • 10.1073/pnas.0802241105

PubMed ID

  • 18606988

Additional Document Info

start page

  • 9769

end page

  • 74

volume

  • 105

number

  • 28