Perfringolysin O Expression in Clostridium perfringens Is Independent of the Upstream pfoR Gene

Abstract

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 .