The production of CAI-1 (Cholerae Autoinducer-1) in Vibrio cholerae is a finely tuned process that is influenced by nutrient availability, particularly glucose concentration. In environments with low glucose levels, the bacterium activates its quorum sensing pathway, primarily through the enzyme CqsA, which catalyzes the synthesis of CAI-1 from (S)-adenosylmethionine (SAM) and decanoyl-coenzyme A. Once synthesized, CAI-1 serves as an autoinducer that diffuses out of the bacterial cell and interacts with the CqsS receptor on neighboring bacteria. This engagement triggers a signaling cascade that activates the response regulator LuxO, which is critical for the regulatory network governing quorum sensing. LuxO subsequently promotes the expression of small regulatory RNAs (sRNAs), particularly the quorum regulatory RNA Qrr. The Qrr sRNAs inhibit hapR, a gene encoding a key transcription factor that represses biofilm formation-associated genes. As hapR levels decline due to the action of Qrr, the repression of biofilm-promoting genes is lifted, thus facilitating the transition of Vibrio cholerae into a biofilm state. This intricate interplay between nutrient conditions, quorum sensing signal production, and regulatory mechanisms highlights the sophisticated strategies employed by Vibrio cholerae to enhance its survival and virulence in fluctuating environments.

Quorum Sensing: Vibrio cholerae Autoinducer-1 Biosynthesis References