Plasmid R46 partially protected Salmonella typhimurium, wild type or uvrB or polA, against the lethal effect of ultraviolet (UV) irradiation, but did not protect recA mutants. The plasmid also increased frequency of UV-induced reversion to His+ in all tested his point mutants (wild type for UV sensitivity), including amber, ochre, UGA, missense, and frame-shift mutants. Plasmid R46 also increased UV-induced reversion to His+ in uvrB and polA strains, but no UV mutagenic effect was detected in R- or R46-carrying recA derivatives of a his (amber) mutant. The spontaneous reversion frequency of his nonsense mutants of all classes, and of some his missense mutants, was increased about 10-fold when the strains carried R46, but the plasmid had no effect on the spontaneous reversion frequency of some other his missense mutations or of reversion rate of his frame-shift mutants (except for two uvrB derivatives of one single-base insertion mutant). The plasmid increased the ability of wild-type, polA, and uvrB hosts to support plaque production by UV-irradiated phage, and made strain LT2 hisG46 less sensitive to methyl methane sulfonate and to X rays and more responsive to the mutagenic effect of visible-light irradiation. R46 increased spontaneous reversion frequency of a his (amber) rec+ strain, but had no such effect in its recA sublines. Since the plasmid in the absence of host recA function fails to produce its mutator effect, or to confer UV protection or to enhance UV mutagenesis, these three effects may be produced via some mechanism involved in recA-dependent deoxyribonucleic acid repair, perhaps by an increase in activity of the "error prone" component of the inducible repair pathway.