MUCAB BUT NOT UMUDC PROTEINS ENHANCE -2-FRAMESHIFT MUTAGENESIS INDUCED BY N-2-ACETYLAMINOFLUORENE AT ALTERNATING GC SEQUENCES

N-2-acetylaminofluorene has been shown efficiently to induce both -1 a nd -2 frameshift mutations in Escherichia coli as well as in mammalian cells. In E. coli, the genetic characteristics of -1 and -2 frameshif t mutations were found to be distinct. The -1 frameshift mutation path way occurs at monotonous runs of G residues (i.e. GGG-->GG). This path way exhibits the same genetic requirements as UV light-induced base su bstitution mutagenesis. Indeed, optimal mutagenesis requires the expre ssion of both UmuDC and the activated form of RecA. The -2 frameshift mutation pathway operates at short alternating GpC sequences, such as the NarI sequence (i.e. GGCGCC-->GGCC), In contrast to the -1 frameshi ft mutation pathway, optimal induction does not require the UmuDC and RecA proteins. This pathway involves a LexA-repressed function tentati vely called Npf (for NarI processing factor). In this paper, we show t hat MucAB efficiently stimulates the -2 frameshift mutation pathway. H owever, unlike the Npf pathway, MucAB-mediated stimulation requires ex pression of the RecA protein.