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Clostridium difficile , a major cause of nosocomial diarrhea and pseudomembranous colitis, still poses serious health-care challenges. The expression of its two main virulence factors, TcdA and TcdB, is reportedly repressed by cysteine, but molecular mechanism remains unclear. The cysteine desulfidase CdsB affects the virulence and infection progresses of some bacteria. The  C. difficile  strain 630 genome encodes a homolog of CdsB, and in the present study, we analyzed its role in  C. difficile  630Δ erm  by constructing an isogenic ClosTron-based  cdsB  mutant. When  C. difficile  was cultured in TY broth supplemented with cysteine, the  cdsB  gene was rapidly induced during the exponential growth phase. The inactivation of  cdsB  not only affected the resistance of  C. difficile  to cysteine, but also altered the expression levels of intracellular cysteine-degrading enzymes and the production of hydrogen sulfide. This suggests that  C. difficile  CdsB is a major inducible cysteine-degrading enzyme. The inactivation of the  cdsB  gene in  C. difficile  also removed the cysteine-dependent repression of toxin production, but failed to remove the Na 2 S-dependent repression, which supports that the cysteine-dependent repression of toxin production is probably attributable to the accumulation of cysteine by-products. We also mapped a δ 54  (SigL)-dependent promoter upstream from the  cdsB  gene, and  cdsB  expression was not induced in response to cysteine in the  cdsR :: ermB  or  sigL :: ermB  strain. Using a reporter gene fusion analysis, we identified the necessary promoter sequence for cysteine-dependent  cdsB  expression. Taken together, these results indicate that CdsB is a key inducible cysteine desulfidase in  C. difficile  which is regulated by δ 54  and CdsR in response to cysteine and that cysteine-dependent regulation of toxin production is closely associated with cysteine degradation.

Novel Cysteine Desulfidase CdsB Involved in Releasing Cysteine Repression of Toxin Synthesis in Clostridium difficile