Sporulation and Enterotoxin Production by Mutants of
            <i>Clostridium perfringens</i>

Duncan, Charles L.; Strong, Dorothy H.; Sébald, M

doi:10.1128/jb.110.1.378-391.1972

Cited by 142 publications

(68 citation statements)

References 34 publications

(38 reference statements)

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“…In contrast, Spo0A directly represses the expression of the cry toxin genes in B. thuringiensis and a spo0A mutant is therefore a hyper-producer of the insecticidal crystal protein [18,21]. In Clostridium perfringens TpeL, a member of the large clostridial toxins just like TcdA and TcdB, is directly dependent on Spo0A [64] and also the production of enterotoxin in this organism seems to be (indirectly) dependent on sporulation [65,66].…”

Section: Regulation Of Toxin Productionmentioning

confidence: 97%

C. difficile 630Δerm Spo0A Regulates Sporulation, but Does Not Contribute to Toxin Production, by Direct High-Affinity Binding to Target DNA

et al. 2012

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Clostridium difficile is a Gram positive, anaerobic bacterium that can form highly resistant endospores. The bacterium is the causative agent of C. difficile infection (CDI), for which the symptoms can range from a mild diarrhea to potentially fatal pseudomembranous colitis and toxic megacolon. Endospore formation in Firmicutes, including C. difficile, is governed by the key regulator for sporulation, Spo0A. In Bacillus subtilis, this transcription factor is also directly or indirectly involved in various other cellular processes. Here, we report that C. difficile Spo0A shows a high degree of similarity to the well characterized B. subtilis protein and recognizes a similar binding sequence. We find that the laboratory strain C. difficile 630Δerm contains an 18bp-duplication near the DNA-binding domain compared to its ancestral strain 630. In vitro binding assays using purified C-terminal DNA binding domain of the C. difficile Spo0A protein demonstrate direct binding to DNA upstream of spo0A and sigH, early sporulation genes and several other putative targets. In vitro binding assays suggest that the gene encoding the major clostridial toxin TcdB may be a direct target of Spo0A, but supernatant derived from a spo0A negative strain was no less toxic towards Vero cells than that obtained from a wild type strain, in contrast to previous reports. These results identify for the first time direct (putative) targets of the Spo0A protein in C. difficile and make a positive effect of Spo0A on production of the large clostridial toxins unlikely.

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Section: Regulation Of Toxin Productionmentioning

confidence: 97%

C. difficile 630Δerm Spo0A Regulates Sporulation, but Does Not Contribute to Toxin Production, by Direct High-Affinity Binding to Target DNA

et al. 2012

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“…Substantial experimental and epidemiological evidence [1,5] now indicates that most, if not all, GI symptoms of these C. perfringens associated diseases are caused by the C. perfringens enterotoxin (CPE). Although several studies [6][7][8][9][10] indicated that CPE synthesis and release is associated with sporulation, this association has never been confirmed by gene knock-out studies. Furthermore, the molecular mechanism of sporulation and its role in CPE synthesis and release has not been studied in great detail at the molecular level.…”

Section: Introductionmentioning

confidence: 98%

Disruption of the gene (spo0A) encoding sporulation transcription factor blocks endospore formation and enterotoxin production in enterotoxigenic Clostridium perfringens type A

Huang

Waters

Grau

et al. 2004

FEMS Microbiology Letters

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This study identified a functional spo0A ORF in enterotoxigenic Clostridium perfringens type A. To evaluate the function of spo0A, an isogenic spo0A knock-out mutant was constructed. The spo0A mutant was unable to form endospores and produce enterotoxin, however, these defects could be restored by complementing the mutant with a recombinant plasmid carrying the wild-type spo0A gene. These results provide evidence that spo0A expression is essential for sporulation and enterotoxin production in C. perfringens.

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“…The symptoms of food poisoning are induced by action of the enterotoxin that is synthesized and released when the ingested vegetative cells undergo sporulation in the intestinal tract. The enterotoxin which is responsible for human food poisoning is only produced during sporulation and not during vegetative growth of this organism (Duncan and Strong 1969; Duncan and Strong 1969a;Duncan et al 1972). T o our knowledge there has been no report where C. perfringens food poisoning was known to have occurred due to ingestion of food containing preformed enterotoxin in the food.…”

Section: Introductionmentioning

confidence: 99%

ENTEROTOXIN FORMATION IN FOODS BY CLOSTRIDIUM PERFRINGENS TYPE A

Naik¹,

Duncan

1977

Journal of Food Safety

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Growth, sporulation and enterotoxin formation in various foods inoculated with a Clostridium perfringens type A enterotoxin‐producing strain were studied. Good vegetative growth, 107–108 cells/g, was obtained after 4 hr of anaerobic growth and remained almost the same throughout the 20–24 hr observation in most of the foods. A gradual increase in spore count to the level of 104–105/g was observed with an increase in the incubation time. Enterotoxin was detected in moist cooked chuck roast, ground beef and turkey as well as in moist cooked and dry roasted chicken at levels up to 0.125μg/g. The earliest time at which enterotoxin was detected was after 10 hr of anaerobic growth in moist cooked turkey at 37°C. Although growth and some sporulation occurred, enterotoxin was not detected in dry roasted beef or turkey with or without gravy, or in moist cooked pork or lamb. Poor growth and sporulation also were obtained with chicken broth, chicken gravy and beef gravy. In moist cooked turkey that had been temperature abused for 6 hr at 37°C, held cold for 15 hr and reheated to 37°C, toxin could be detected after only 5 hr of holding at 37°C. The ability of certain foods to support sporulation and enterotoxin formation indicates that such preformed enterotoxin may contribute to early onset of symptoms in some cases of C. perfringens food poisoning.

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Sporulation and Enterotoxin Production by Mutants of Clostridium perfringens

Cited by 142 publications

References 34 publications

C. difficile 630Δerm Spo0A Regulates Sporulation, but Does Not Contribute to Toxin Production, by Direct High-Affinity Binding to Target DNA

C. difficile 630Δerm Spo0A Regulates Sporulation, but Does Not Contribute to Toxin Production, by Direct High-Affinity Binding to Target DNA

Disruption of the gene (spo0A) encoding sporulation transcription factor blocks endospore formation and enterotoxin production in enterotoxigenic Clostridium perfringens type A

ENTEROTOXIN FORMATION IN FOODS BY CLOSTRIDIUM PERFRINGENS TYPE A

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