Abstract
Assessing the regulation of Clostridium difficile transferase (CDT), is complicated by the presence of a Pathogenicity locus (PaLoc) which encodes Toxins A and B. Here we developed R20291ΔPaLoc model strains and cell-based assays to quantify CDT-mediated virulence. Their application demonstrated that the transcriptional regulator, CdtR, was required for CDT-mediated cytotoxicity.
Highlights
Assessing the regulation of Clostridium difficile transferase (CDT), is complicated by the presence of a Pathogenicity locus (PaLoc) which encodes Toxins A and B
The main virulence factors of C. difficile are Toxin A (TcdA) and Toxin B (TcdB) whose genes reside on a 19.6 Kb pathogenicity locus (PaLoc) [2]
Some hypervirulent strains responsible for outbreaks and severe cases of disease, in particular BI/NAP1/027 strains including the archetypal strain R20291, produce an additional toxin, the binary toxin or Clostridium difficile transferase (CDT) [3]
Summary
Assessing the regulation of Clostridium difficile transferase (CDT), is complicated by the presence of a Pathogenicity locus (PaLoc) which encodes Toxins A and B. We developed R20291DPaLoc model strains and cell-based assays to quantify CDT-mediated virulence. A gene encoding the transcriptional regulator CdtR belonging to the LytTR family, was discovered upstream of cdtA and cdtB (for locus arrangement see Fig. S1b), and was shown to be required for the maximal expression of CDT [5].
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