Figure 5.

V. cholerae QS circuit. V. cholerae detects CAI-1 (produced by CqsA) and AI-2 (produced by LuxS) via two two-component histidine kinases, CqsS and LuxPQ, respectively. In the absence of AIs at LCD, the receptors function as kinases resulting in phosphorylation of LuxO, via LuxU, and activation of qrr gene expression. The Qrr sRNAs activate aphA and repress hapR expression. AphA represses hapR and activates tcpPH. TcpPH activates toxT expression and ToxT activates expression of the major virulence factors. At HCD, AIs bind the receptors switching them to phosphatases resulting in dephosphorylation of LuxO, cessation of qrr gene expression, and increased hapR expression. HapR represses aphA to shut down virulence factor production.