Vibrio cholerae, the causative agent of the human disease cholera, uses cell-to-cell communication to control pathogenicity and biofilm formation. This process, known as quorum sensing, relies on the secretion and detection of signalling molecules called autoinducers. At low cell density V. cholerae activates the expression of virulence factors and forms biofilms. At high cell density the accumulation of two quorum-sensing autoinducers represses these traits. These two autoinducers, cholerae autoinducer-1 (CAI-1) and autoinducer-2 (AI-2), function synergistically to control gene regulation, although CAI-1 is the stronger of the two signals. V. cholerae AI-2 is a furanosyl borate diester, which was identified and fully characterized in Vibrio harveyi.    CAI-1 is (S)-3- hydroxytridecan-4-one, a new type of bacterial signal.  The structure elucidation, synthesis, mechanism of action,  and structure-activity relations for both AI-2 and CAI-1 will be discussed.   CAI-1 represses production of the canonical virulence factor TCP (toxin co-regulated pilus) which suggests that CAI-1 could be used as a therapy to prevent cholera infection and, furthermore, that strategies to manipulate bacterial quorum sensing hold promise in the clinical arena.