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J Bacteriol. 1972 April; 110(1): 378-391
Copyright © 1972 American Society for Microbiology. All Rights Reserved.

Sporulation and Enterotoxin Production by Mutants of Clostridium perfringens

Food Research Institute and Department of Bacteriology, University of Wisconsin, Madison, Wisconsin 53706, and Laboratoire des Anaerobies, Institut Pasteur, Paris, France

ABSTRACT

The ability of Clostridium perfringens type A to produce an enterotoxin active in human food poisoning has been shown to be directly related to the ability of the organism to sporulate. Enterotoxin was produced only in a sporulation medium and not in a growth medium in which sporulation was repressed. Mutants with an altered ability to sporulate were isolated from an sp⁺ ent⁺ strain either as spontaneous mutants or after mutagenesis with acridine orange or nitrosoguanidine. All sp₀^– mutants were ent^–. Except for one isolate, these mutants were not disturbed in other toxic functions characteristic of the wild type and unrelated to sporulation. A total of four of seven osp₀ mutants retained the ability to produce detectable levels of enterotoxin. None of the ent^– mutants produced gene products serologically homologous to enterotoxin. A total of three sp^– mutants, blocked at intermediate stages of sporulation, produced enterotoxin. Of these mutants, one was blocked at stage III, one probably at late stage IV, and one probably at stage V. A total of three sp⁺ revertants isolated from an sp^– ent^– mutant regained not only the ability to sporulate but also the ability to produce enterotoxin. The enterotoxin appears to be a sporulation-specific gene product; however, the function of the enterotoxin in sporulation is unknown.

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