Excision-repair in mutants of Escherichia coli deficient in DNA polymerase I and/or its associated 5' leads to 3' exonuclease

Mol Gen Genet. 1977 Jan 7;150(1):1-12. doi: 10.1007/BF02425319.


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.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • DNA Polymerase I / metabolism*
  • DNA Repair*
  • DNA, Bacterial / biosynthesis
  • DNA, Bacterial / metabolism*
  • DNA-Directed DNA Polymerase / metabolism*
  • Escherichia coli / enzymology
  • Escherichia coli / metabolism*
  • Escherichia coli / radiation effects
  • Genes
  • Models, Biological
  • Mutation
  • Pyrimidine Dimers / metabolism
  • Ultraviolet Rays


  • DNA, Bacterial
  • Pyrimidine Dimers
  • DNA Polymerase I
  • DNA-Directed DNA Polymerase