DETECTION OF OXIDATIVE MUTAGENS IN STRAINS OF ESCHERICHIA-COLI DEFICIENT IN THE OXYR OR MUTY FUNCTIONS - DEPENDENCE ON SOS MUTAGENESIS

The Escherichia coli strain IC3821, a Delta oxyR derivative of WP2 uvr A trpE65, was more sensitive to mutagenicity promoted by t-butyl hydro peroxide and cumene hydroperoxide than the isogenic oxyR(+) control. M utagenicity of menadione, a redox cycling quinone, was clearly detecte d in the Delta oxyR strain, whereas only a slight mutagenic response w as observed in the oxyR(+) strain. Plumbagin, another quinone structur ally similar to menadione, was not mutagenic to any of the strains. Th ese mutagenic responses appeared to involve the SOS processing of oxid ative DNA lesions and were mediated by MucA/B proteins more efficientl y than by UmuD/C. In cells lacking mutagenesis proteins, induction of SOS-independent mutations by the two alkyl hydroperoxides required a d eficiency in the MutY DNA glycosylase and was increased by the presenc e of the Delta oxyR mutation. In contrast, the two quinones assayed we re unable to induce SOS-independent mutations in the MutY-deficient st rains.