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Category: Bacterial Pathogenesis
Toxin and Virulence Regulation in Vibrio cholerae, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555818524/9781555816766_Chap12-1.gif /docserver/preview/fulltext/10.1128/9781555818524/9781555816766_Chap12-2.gifAbstract:
Of the more than 200 different serogroups of Vibrio cholerae that have been isolated, only two of these, O1 and O139, have been found to have epidemic and pandemic potential. CTXφ carries the genes for CT (ctxA and ctxB) and the VPI contains the genes (tcpA-E and tcpJ) responsible for the synthesis and assembly of the essential colonization factor toxin-coregulated pilus (TCP). As part of the acetoin operon, AphA represses the expression of two PhoB-activated genes, acgA and acgB, that encode proteins which influence motility and biofilm formation by altering c-di-GMP levels in the cell. Bicarbonate may be an important in vivo signal that increases the activity of ToxT during infection and induces virulence gene expression. Once V. cholerae has disseminated out of the host and virulence gene expression is no longer required, TcpP and ToxT levels are decreased by proteolysis and H-NS reestablishes repression at the various promoters. Thus, like GbpA, FrhA plays an important role in V. cholerae in both the host and in the aquatic environment. A model for V. cholerae infection involves motile bacteria attaching to the intestinal cell surface, after which they upregulate virulence factor expression and downregulate motility. The flagellar regulatory hierarchy also influences virulence gene expression in V. cholerae through the quorum sensing system. Recent advances in the development of cDNA sequencing (RNA-seq) have facilitated the generation of comprehensive transcriptome profiles of V. cholerae during infection in both the rabbit and mouse models of cholera.
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The Vibrio cholerae virulence cascade. The VPI is shown by a blue line, CTXΦ by a red line, and the ancestral genome by black lines. At low cell density, in the absence of CAI-1 and AI-2, CqsS and LuxPQ phosphorylate LuxO, which, together with σ54, activates the expression of qrr1 to qrr4. The resulting small RNAs, together with Hfq, destabilize the hapR message, leading to activation of aphA expression by Lrp and VpsR. AphA cooperates with AphB to activate the tcpPH promoter. TcpPH cooperates with ToxRS to activate the toxT promoter. ToxT then activates the tcpA and ctx promoters. At low cell density, AphA also represses the expression of qrr2 to -4 and hapR. At high cell density, in the presence of CAI-1 and AI-2, LuxO is not phosphorylated and qrr1 to qrr4 are not expressed. This allows for the accumulation of HapR, which binds to a site in the aphA promoter overlapping the VpsR binding site, repressing its expression and turning off the virulence cascade. doi:10.1128/9781555818524.ch12f1
The Vibrio cholerae virulence cascade. The VPI is shown by a blue line, CTXΦ by a red line, and the ancestral genome by black lines. At low cell density, in the absence of CAI-1 and AI-2, CqsS and LuxPQ phosphorylate LuxO, which, together with σ54, activates the expression of qrr1 to qrr4. The resulting small RNAs, together with Hfq, destabilize the hapR message, leading to activation of aphA expression by Lrp and VpsR. AphA cooperates with AphB to activate the tcpPH promoter. TcpPH cooperates with ToxRS to activate the toxT promoter. ToxT then activates the tcpA and ctx promoters. At low cell density, AphA also represses the expression of qrr2 to -4 and hapR. At high cell density, in the presence of CAI-1 and AI-2, LuxO is not phosphorylated and qrr1 to qrr4 are not expressed. This allows for the accumulation of HapR, which binds to a site in the aphA promoter overlapping the VpsR binding site, repressing its expression and turning off the virulence cascade. doi:10.1128/9781555818524.ch12f1
Environmental factors influencing virulence gene expression a
Environmental factors influencing virulence gene expression a