title: Perfringolysin O expression in Clostridium perfringens is independent of the upstream pfoR gene.
abstract: The pathogenesis of Clostridium perfringens-mediated gas gangrene or clostridial myonecrosis involves the extracellular toxins alpha-toxin and perfringolysin O. Previous studies (T. Shimizu, A. Okabe, J. Minami, and H. Hayashi, Infect. Immun. 59:137-142, 1991) carried out with Escherichia coli suggested that the perfringolysin O structural gene, pfoA, was positively regulated by the product of the upstream pfoR gene. In an attempt to confirm this hypothesis in C. perfringens, a pfoR-pfoA deletion mutant was complemented with isogenic pfoA(+) shuttle plasmids that varied only in their ability to encode an intact pfoR gene. No difference in the ability to produce perfringolysin O was observed for C. perfringens strains carrying these plasmids. In addition, chromosomal pfoR mutants were constructed by homologous recombination in C. perfringens. Again no difference in perfringolysin O activity was observed. Since it was not possible to alter perfringolysin O expression by mutation of pfoR, it was concluded that the pfoR gene product is unlikely to have a role in the regulation of pfoA expression in C. perfringens.
authors.affiliation: Bacterial Pathogenesis Research Group, Department of Microbiology, Monash University, Victoria 3800, Australia.
authors.forename: Milena M
authors.initials: MM
authors.lastname: Awad
authors.forename: Julian I
authors.initials: JI
authors.lastname: Rood
mesh_terms: D001427:Bacterial Toxins / Q000096:biosynthesis*; D002876:Chromosomes, Bacterial; D003016:Clostridium perfringens / Q000235:genetics / Q000378:metabolism*; D017353:Gene Deletion; D015870:Gene Expression; D005798:Genes, Bacterial / Q000502:physiology; D005816:Genetic Complementation Test; D006460:Hemolysin Proteins; D015534:Trans-Activators / Q000502:physiology
chemical_list: D001427:Bacterial Toxins; D006460:Hemolysin Proteins; D015534:Trans-Activators; C020452:Clostridium perfringens theta-toxin