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: Milena M Awad, Julian I Rood
• Journal: Journal of bacteriology (J Bacteriol) Vol. 184 Issue 7 Pg. 2034-8 (Apr 2002) ISSN: 0021-9193 [Print] United States
• PMID: 11889112 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Bacterial Toxins
• Hemolysin Proteins
• Trans-Activators
• Clostridium perfringens theta-toxin

Topics

• Bacterial Toxins (biosynthesis)
• Chromosomes, Bacterial
• Clostridium perfringens (genetics, metabolism)
• Gene Deletion
• Gene Expression
• Genes, Bacterial (physiology)
• Genetic Complementation Test
• Hemolysin Proteins
• Trans-Activators (physiology)