Excision-repair in mutants of Escherichia coli deficient in DNA polymerase I and/or its associated 5' leads to 3' exonuclease.
The ultraviolet (UV) sensitivity of Escherichia coli mutants deficient in the 5' leads to 3' exonuclease activity of DNA polymerase I is intermediate between that of pol+ strains and mutants which are deficient in the polymerizing activity of pol I (polA1). Like polA1 mutants, the 5'-exonclease deficient mutants exhibit increased UV-induced DNA degradation and increased repair synthesis compared to a pol+ strain, although the increase is not as great as in polA1 or in the conditionally lethal mutant BT4113ts deficient in both polymerase I activities. When dimer excision was measured at UV doses low enough to avoid interference from extensive DNA degradation, all three classes of polymerase I deficient mutants were found to remove dimers efficiently from their DNA. We conclude that enzymes alternative to polymerase I can operate in both the excision and resynthesis steps of excision repair and that substitution for either of the polymerase I functions results in longer patches of repair. A model is proposed detailing the possible events in the alternative pathways.
D004256:DNA Polymerase I / Q000378:metabolism*; D004260:DNA Repair; D004269:DNA, Bacterial / Q000096:biosynthesis / Q000378:metabolism*; D004259:DNA-Directed DNA Polymerase / Q000378:metabolism*; D004926:Escherichia coli / Q000201:enzymology / Q000378:metabolism* / Q000528:radiation effects; D005796:Genes; D008954:Models, Biological; D009154:Mutation; D011740:Pyrimidine Dimers / Q000378:metabolism; D014466:Ultraviolet Rays
D004269:DNA, Bacterial; D011740:Pyrimidine Dimers; D004256:DNA Polymerase I; D004259:DNA-Directed DNA Polymerase