CodY Promotes Sporulation and Enterotoxin Production by Clostridium perfringens Type A Strain SM101.

type D strains cause enterotoxemia and enteritis in livestock via epsilon toxin production. In type D strain CN3718, CodY was previously shown to increase the level of epsilon toxin production and repress sporulation. type A strains producing enterotoxin (CPE) cause human food poisoning and antibiotic-associated diarrhea. Sporulation is critical for type A food poisoning since spores contribute to transmission and resistance in the harsh food environment and sporulation is essential for CPE production. Therefore, the current study asked whether CodY also regulates sporulation and CPE production in SM101, a derivative of type A food-poisoning strain NCTC8798. An isogenic -null mutant of SM101 showed decreased levels of spore formation, along with lower levels of CPE production. A complemented strain recovered wild-type levels of both sporulation and CPE production. When this result was coupled with the earlier results obtained with CN3718, it became apparent that CodY regulation of sporulation varies among different strains. Results from quantitative reverse transcriptase PCR analysis clearly demonstrated that, during sporulation, transcript levels remained high in SM101 but rapidly declined in CN3718. In addition, gene expression patterns varied significantly between -null mutants of SM101 and CN3718. Compared to the levels in their wild-type parents, the level of gene expression decreased in the CN3718 -null mutant strain but significantly increased in the SM101 -null mutant strain, demonstrating CodY-dependent regulation differences in expression between these two strains. This difference appears to be important since overexpression of the gene in SM101 reduced the levels of sporulation and enterotoxin production, supporting the involvement of AbrB repression in regulating sporulation.