Correlations between carbon metabolism and virulence in bacteria.

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Poncet, Sandrine | Milohanic, Eliane | Mazé, Alain | Abdallah, Jamila Nait | Ake, Françine | Larribe, Mireille | Deghmane, Ala-Eddine | Taha, Muhamed-Kheir | Dozot, Marie | de Bolle, Xavier | Letesson, Jean-Jacques | Deutscher, Josef

Edité par CCSD ; S. Karger -

International audience. Bacteria have developed several mechanisms which allow the preferred utilization of the most efficiently metabolizable carbohydrates when these organisms are exposed to a mixture of carbon sources. Interestingly, the same or similar mechanisms are used by some pathogens to control various steps of their infection process. The efficient metabolism of a carbon source might serve as signal for proper fitness. Alternatively, the presence of a specific carbon source might indicate to bacterial cells that they thrive in infection-related organs, tissues or cells and that specific virulence genes should be turned on or switched off. Frequently, virulence gene regulators are affected by changes in carbon source availability. For example, expression of the gene encoding the Streptococcus pyogenes virulence regulator Mga is controlled by the classical carbon catabolite repression (CCR) mechanism operative in Firmicutes. The activity of PrfA, the major virulence regulator in Listeria monocytogenes, seems to be controlled by the phosphorylation state of phosphotransferase system(PTS) components. In Vibrio cholerae synthesis of HapR, which regulates the expression of genes required for motility, is controlled via the Crp/cAMP CCR mechanism, whereas synthesis of Salmonella enterica HilE, which represses genes in a pathogenicity island, is regulated by the carbohydrate-responsive, PTS-controlled Mlc.

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