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© Michel-Robert Popoff
Clostridium difficile en microscopie à contraste de phase. On distingue des bactéries sporulées, non sporulées et d'autres en cours de lyse (destruction). Bactérie de l'environnement (sol, eau, foin, sable), elle est à l'origine d'infections nosocomiales survenant après un traitement antibiotique : Clostridium difficile prédomine alors que les autres bactéries de la flore intestinale ont été détruites. L'infection peut provoquer deux types de pathologies graves : les colites pseudo-membraneuses dont l'origine est quasiment due à 100 % à C. difficile et la diarrhée post-antibiothérapie due à C. difficile dans 30 % des cas de ces diarrhées.
Publication : Molecular microbiology

CcpA-mediated repression of Clostridium difficile toxin gene expression

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Molecular microbiology - 28 Dec 2010

Antunes A, Martin-Verstraete I, Dupuy B

Link to Pubmed [PMID] – 21299645

Mol. Microbiol. 2011 Feb;79(4):882-99

The presence of glucose or other rapidly metabolizable carbon sources in the bacterial growth medium strongly represses Clostridium difficile toxin synthesis independently of strain origin. In Gram-positive bacteria, carbon catabolite repression (CCR) is generally regarded as a regulatory mechanism that responds to carbohydrate availability. In the C. difficile genome all elements involved in CCR are present. To elucidate in vivo the role of CCR in C. difficile toxin synthesis, we used the ClosTron gene knockout system to construct mutants of strain JIR8094 that were unable to produce the major components of the CCR signal transduction pathway: the phosphotransferase system (PTS) proteins (Enzyme I and HPr), the HPr kinase/phosphorylase (HprK/P) and the catabolite control protein A, CcpA. Inactivation of the ptsI, ptsH and ccpA genes resulted in derepression of toxin gene expression in the presence of glucose, whereas repression of toxin production was still observed in the hprK mutant, indicating that uptake of glucose is required for repression but that phosphorylation of HPr by HprK is not. C. difficile CcpA was found to bind to the regulatory regions of the tcdA and tcdB genes but not through a consensus cre site motif. Moreover in vivo and in vitro results confirmed that HPr-Ser45-P does not stimulate CcpA-dependent binding to DNA targets. However, fructose-1,6-biphosphate (FBP) alone did increase CcpA binding affinity in the absence of HPr-Ser45-P. These results showed that CcpA represses toxin expression in response to PTS sugar availability, thus linking carbon source utilization to virulence gene expression in C. difficile.

https://www.ncbi.nlm.nih.gov/pubmed/21299645