Summary: PAO lacks UV-inducible Weigle reactivation and Weigle mutagenesis of UV-damaged bacteriophages. This lack of UV-inducible, error-prone DNA repair appears to be due to the absence of efficiently expressed -like genes in this species. When the gene is introduced into a (Def) mutant of K12, the gene product is capable of mediating UV-induced mutagenesis, indicating that it could participate in a -like regulatory network and function in inducible DNA repair pathways if such existed in . The presence of the IncP9, UV-resistance plasmid R2 in RecA strains of PAO allows UV-inducible, mutagenic DNA repair of UV-irradiated bacteriophages. R2 also greatly stimulates the ability of UV radiation to induce mutagenesis of the bacterial chromosome. When R2 is introduced into strains containing either the or mutation, plasmid-mediated UV resistance and Weigle reactivation are not observed. These observations suggest that the increased protection afforded to by R2 is derived from a RecA-mediated, DNA-damage-inducible, error-prone DNA repair system which complements the lack of a chromosomally encoded -like operon.


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