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. 2012 Jun 28;8(6):e1002767. doi: 10.1371/journal.ppat.1002767

Figure 1. The Quorum-Sensing Circuit in Vibrio cholerae.

Figure 1

The CqsA/CqsS signal transduction system is shown as the example for the V. cholerae QS circuit. (Left) At low cell density (LCD), the CAI-1 autoinducer concentration is below the detection threshold, and the membrane bound CqsS receptor functions as a kinase. The LuxO response regulator is phosphorylated and it activates the transcription of genes encoding the four Qrr sRNA genes. Aided by the RNA chaperone Hfq, the Qrr sRNAs activate and repress translation of the AphA and HapR proteins, respectively. (Right) At high cell density (HCD), binding of CAI-1 to CqsS inhibits its kinase activity. LuxO is not phosphorylated and transcription of the qrr genes is terminated. Translation of AphA is inhibited and HapR is derepressed. Hundreds of genes are controlled by AphA and HapR, including genes required for biofilm formation and virulence. HapR also functions as a transcriptional activator of the heterologous V. harveyi lux operon [22], [24], [26]–[30]. Dotted lines denote components that are not expressed while solid lines represent those that are produced.