The antitumour drug nitracrine [1-nitro-9-(dimethylaminopropylamino)acridine], known to be a potent frameshift mutagen in strains of Salmonella typhimurium, also strongly reverts the lacZ19124 frameshift marker in Escherichia coli. The results in E. coli indicate that nitracrine causes DNA damage which can be excised by the UvrA,B,C excinuclease, can generate mutations by a recA-dependent mechanism, and gives enhanced yields of mutants when plasmid pKM101 is present. Despite these observations, mutagenesis by nitracrine appears to be independent of the UmuC gene product, and hence nitracrine differs from most (but not all) other chemicals which generate mutations via the SOS response. Given that umuC mutants are about as mutable by nitracine as the wild-type parent strain, it is somewhat surprising that plasmid pKM101 causes an enhancement of nitracrine mutagenesis. Nevertheless, we have found that the observed enhancement of mutagenesis by pKM101 is a function of the mucB gene, normally assumed to be essentially homologous to the umuC gene.