Proceedings of the National Academy of Sciences · 1988 · 53 citations · 28 references
Life SciencesGeneticsMolecular BiologyDna RepairGenetic EngineeringMicrobial GeneticsDna Polymerase FunctionPlasmid BiologyPlasmid EngineeringPlasmid GeneticsRecombinant Plasmid ConstructionDna Polymerase IiiEscherichia ColiMutagenic EffectivenessMutagenic MechanismsMutator AllelesMutator PhenotypesUv-induced Dna Lesions
It has been found that the mutator phenotype of the recA441 and recA730 strains that express the SOS response constitutively is suppressed by pIP1, a high-copy plasmid carrying the dnaQ gene encoding the 3'----5' exonuclease subunit (epsilon) of DNA polymerase III. We have constructed plasmid pIP11, in which the dnaQ gene is fused to the strong tac (trp-lac) promoter. Enhanced synthesis of the epsilon subunit stimulated by isopropyl beta-D-thiogalactopyranoside, the inducer of tac, prevents expression of the mutator phenotype of recA441 and markedly decreases the frequency of UV-induced mutations. These results strongly suggest that a loss of editing capacity by the epsilon subunit of DNA polymerase III holoenzyme plays a crucial role in generation of mutations during the SOS response.
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