Inhibition of DNA replication in E. coli results in coordinate expression of a cluster of diverse functions, including prophage induction and filamentous growth, many of which are thermally inducible, without inhibition of DNA synthesis, in strains carrying a mutation in the "tif" locus. It has been proposed that one of the inducible functions in this cluster is responsible for the ultraviolet mutability of E. coli. As a test of this hypothesis, the effect of postirradiation temperature elevation on ultraviolet mutability was compared in strains differing by a tif mutation. In a tif+ strain, raising the temperature to 420 after irradiation did not change the frequency of induced mutations to tryptophan-independence. Similar treatment of a tif-1 strain resulted in as much as a 10-fold increase in the induced mutation yield. Thermal enhancement of ultraviolet mutability in the tif-1 strain was prevented or promoted by agents known to exert parallel effects on thermal induction of lambda prophage in tif lysogens. The results support the hypothesis that ultraviolet mutability in E. coli depends upon an inducible function that is normally expressed only when DNA replication is inhibited.Properties of Escherichia coli strains lacking DNA polymerase I (1, 2) support the hypothesis (3, 4) that a function necessary for ultraviolet (UV) mutagenesis is inducible, and that its induction has the same requirements as a number of other UVinducible functions, exemplified by induction of prophage lambda. These requirements normally include a recA + lex + genotype and conditions under which DNA replication is inhibited while RNA and protein synthesis continue. However, in tif mutant strains of E. coli K12, prophage induction, filamentous growth, W-reactivation, and W-mutagenesis (see Abbreviations) (5) detected? Since UV-induced mutations are believed to originate as errors in the repair of daughter-strand gaps opposite unexcised pyrimidine dimers (9, 10), the postulated inducible function may have no demonstrable effects in unirradiated cells, which contain no such gaps. Irradiated bacteria, therefore, must be used to detect thermally induced UV mutability. However, since all but the lowest doses of UV are themselves efficient inducers of UV-inducible functions, presumably including the one in question, a test for thermal induction of UV mutability must be conducted only with cells exposed to extremely low doses of UV. In uvrA strains, doses below about 5 ergs/mm2 induce very little prophage, (11) and promote very little W-reactivation (3). Irradiation of uvrA tif bacteria with UV doses in this low range, therefore, should introduce some pyrimidine dimers capable of producing daughter-strand gaps (about 6 per erg/mm2 per E. coli genome) without also inducing the capacity to effect UV mutagenesis in more than a very small fraction of the population, thus providing conditions necessary for a biological assay of thermal inducibility of this capacity. The hypothesis that UV mutagenesis depends upon an inducible function gen...