The isfA mutation specifically inhibits the SOS-dependent mutagenic pathway and does not selectively affect any particular base substitution

We have previously described a new mutation in Escherichia coli, isfA, whic h causes inhibition of SOS mutagenesis (UV-induced in reef and spontaneous in recA730 strains) and several SOS-dependent phenomena. Antimutagenic acti vity of the isfA mutation in the recA730 strain was shown to be related to inhibition of processing of UmuD to UmuD' by RecA* coprotease. In the prese nt study we have analysed the specificity of the antimutagenic activity of the isfA mutation by employing F' plasmids carrying a set of mutant lacZ ge nes that can individually detect two types of transitions and four types of transversions, Analysis revealed that isfA inhibits UV-induced G:C --> A:T and A:T --> G:C transitions, but does not affect the same G:C --> A:T tran sitions induced by EMS, an SOS-independent mutagen. Analysis of the antimut agenic activity of the isfA mutation in two mutator strains, recA730 and mu tL, showed that isfA inhibits SOS-dependent transversions in recA730, but n ot transitions generated as replication errors in the mutL strain. In the d ouble mutant recA730 mutL, both transitions and transversions were enhanced and isfA inhibits most transversions and only those transitions generated by the recA730 mutation. The results indicate that the antimutagenic activi ty of the isfA mutation is specific for the SOS, UmuD'C-dependent mutagenic pathway but does not selectively affect any particular base substitution. Moreover, studies on the effect of the isfA mutation on transitions and tra nsversions in different genetic backgrounds enable us to recognize differen t mutagenic pathways active in recA730 cells.