GSE115711
Three autoinducer molecules act synergistically to control virulence gene expression in Vibrio cholerae [dataset 1]
Bacteria use quorum sensing (QS) to monitor cell density and coordinate group behaviours. In Vibrio cholerae, the causative agent of cholera disease, QS is linked to virulence gene expression via the autoinducer molecules, AI-2 and CAI-1. Both autoinducers share one signal transduction pathway to control AphA production, a key transcriptional activator of virulence genes. In this study, we demonstrate that the recently identified autoinducer, DPO, also controls AphA production in V. cholerae. DPO acts through the transcriptional activator, VqmA, and the VqmR small RNA to reduce AphA levels at the post-transcriptional level. Consequently, DPO inhibits virulence gene expression in V. cholerae, including repression of the cholera toxin, a key factor required for disease in humans. VqmR-mediated repression of AphA links the AI-2/CAI-1 and DPO-dependent QS pathways of V. cholerae and global transcriptome analysis indicate that all three autoinducers are required for full QS function. Together, our data provide the first view on autoinducer interplay in V. cholerae and highlight the importance of post-transcriptional gene regulation for collective functions in this major human pathogen. Overall design: mRNA expression profiles of a V. cholerae strain deficient for autoinducer synthesis and induced with the corresponding autoinducers. Three independent biological replicates for each treatment with single autoinducers as well as all possible combinations are provided. The bacteria were grown in M9 minimal media in the presence of 5µM final concentration of the autoinducers: autoinducer 2 (AI-2), cholera-autoinducer-1 (CAI-1), or 3,5-dimethylpyrazin-2-ol (DPO), or water (control). The following day, bacteria were diluted 1:500 in fresh media with the same composition and RNA samples were collected at low optical density.