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. 2014 Dec 24;14:327. doi: 10.1186/s12866-014-0327-y

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© Lo Scrudato et al.; licensee BioMed Central. 2014

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Proposed working model describing the transcriptional regulation of the competence genes qstR and comEA within the network of natural competence for transformation of V. cholerae . qstR and comEA are tightly regulated by three different pathways: quorum sensing, chitin-sensing/degradation, and carbon catabolite repression (signals indicated on top; from left to right). Upon growth on chitin or artifical induction, TfoX is produced within the cell. Furthermore, unsaturated PTS systems lead to the activation of the enzyme adenylate cyclase, which synthesizes cAMP. cAMP then forms a complex with CRP. Based on work performed in H. influenzae [20,21], we hypothesized that CRP-cAMP might bind to the putative CRP-S sites described here and that such binding would be dependent on TfoX. However, full expression of those genes requires a QS-dependent secondary activator (HapR and QstR, respectively). At high cell density the master regulator of QS, HapR, is produced and allows the expression of qstR by directly binding to its promoter (indicated by an asterisk marking a HapR binding site identified in vitro; [22]. The transcriptional regulator QstR, which might require a cofactor for its full activity (indicated by the triangle), positively regulates the comEA gene potentially by binding to a QstR-specific binding motif (indicated by the dashed box and so far unidentified). The question marks indicate the subjects addressed in this study.