Learn More
AphA is a quorum sensing-regulated activator that initiates the virulence cascade in Vibrio cholerae by cooperating with the LysR-type regulator AphB at the tcpPH promoter on the Vibrio pathogenicity island (VPI). To identify the ancestral chromosomal genes in V. cholerae regulated by AphA, we carried out a microarray analysis and show here that AphA(More)
Quorum sensing negatively influences virulence gene expression in certain toxigenic Vibrio cholerae strains. At high cell densities, the response regulator LuxO fails to reduce the expression of HapR, which, in turn, represses the expression of the virulence cascade. A critical regulatory step in the cascade is activation of tcpPH expression by AphA and(More)
We describe here a new member of the LysR family of transcriptional regulators, AphB, which is required for activation of the Vibrio cholerae ToxR virulence cascade. AphB activates the transcription of the tcpPH operon in response to environmental stimuli, and this process requires cooperation with a second protein, AphA. The expression of neither aphA or(More)
The expression of the Vibrio cholerae virulence factors, toxin-co-regulated pilus (TCP) and cholera toxin (CT), are dependent on the ability of the LysR regulator AphB to co-operate with a second protein, AphA, to activate the expression of the membrane-bound transcription factors TcpP and TcpH. To gain insights into the mechanism by which AphA and AphB(More)
HapR is a quorum sensing-regulated transcription factor that represses the virulence cascade in Vibrio cholerae by binding to a specific site centred at -71 in the aphA promoter, ultimately preventing activation of the tcpPH promoter on the Vibrio pathogenicity island. In an effort to elucidate the mechanism by which HapR represses aphA expression, we(More)
Activation of the tcpPH promoter on the Vibrio pathogenicity island by AphA and AphB initiates the Vibrio cholerae virulence cascade and is regulated by quorum sensing through the repressive action of HapR on aphA expression. To further understand how the chromosomally encoded AphA protein activates tcpPH expression, site-directed mutagenesis was used to(More)
The alternative sigma factor sigma(E) (RpoE) is involved in the response to extracytoplasmic stress and plays a role in the virulence of a variety of different bacteria. To assess the role of sigma(E) in Vibrio cholerae pathogenesis, a DeltarpoE mutant was constructed and analyzed using the infant mouse model. The results here show that sigma(E) contributes(More)
AphA is required for expression of the Vibrio cholerae virulence cascade and for its regulation by quorum sensing. In order to activate transcription, AphA functions together with a second protein, the LysR-type regulator AphB, at the tcpPH promoter. As AphA is a member of a new and largely uncharacterized regulator family, random mutagenesis was used to(More)
Vibrio cholerae strains of the classical biotype express the genes encoding cholera toxin (CT) and toxin-coregulated pilus (TCP) under a variety of environmental conditions in vitro, whereas El Tor biotype strains express these genes only under specialized culture conditions. We show here that a single base-pair difference at positions -65 and -66 of the(More)
Virulence gene expression in Vibrio cholerae is dependent upon a complex transcriptional cascade that is influenced by both specific and global regulators in response to environmental stimuli. Here, we report that the global regulator integration host factor (IHF) positively affects virulence gene expression in V. cholerae. Inactivation of ihfA and ihfB,(More)