The LuxM, LuxS and CqsA enzymes synthesise the signal molecules HAI-1, AI-2 and CAI-1, respectively. These signal molecules are detected at the cell surface by the LuxN, LuxQ and CqsS two-component receptor proteins, respectively. Detection of AI-2 by LuxQ requires the periplasmic protein LuxP. (A) In the absence of signal molecules, the receptors autophosphorylate and transfer phosphate to LuxO via LuxU. Phosphorylation activates LuxO, which together with σ54 activates the production of five small regulatory RNAs (sRNAs). These sRNAs, together with the chaperone Hfq, destabilise the mRNA encoding the transcriptional regulator LuxR. Therefore, in the absence of autoinducers, the LuxR protein is not produced. LuxR is a repressor of ExsA. Hence, in the absence of signal molecules, ExsA is produced and in turn activates expression of the TTSS operons. (B) In the presence of high concentrations of the signal molecules, the receptor proteins switch from kinases to phosphatases, which results in dephosphorylation of LuxO. Dephosphorylated LuxO is inactive and therefore, the sRNAs are not formed and the transcriptional regulator LuxR is produced. LuxR represses ExsA, and the TTSS operons are not expressed. “P” denotes phosphotransfer.