Trimethoprim-induced DNA polymerase I deficiency in Escherichia coli K-12

J Bacteriol. 1983 Jun;154(3):1098-103. doi: 10.1128/jb.154.3.1098-1103.1983.

Abstract

Curing of the mini-ColE1 plasmid pML21 was observed among cells of Escherichia coli K-12 strain C600(pML21) grown under subinhibitory conditions in the presence of trimethoprim, a specific inhibitor of dihydrofolate reductase. Some of the cured colonies showed (i) a reduction in frequency of transformation with pML21 compared with those of isogenic strains not treated with trimethoprim, (ii) loss of viability after acquisition of a recA mutation, and (iii) UV sensitivity greater than that of the original isogenic strain. These colonies therefore had PolA- phenotypes. Moreover, they were found to be deficient in DNA polymerase I activity in the in vitro assays, indicating the occurrence of a polA mutation in them. Many of the colonies with PolA- phenotypes were also thyA deoC mutants, and these mutations, in addition to the polA mutations, appeared to be involved in the expression of the PolA- phenotypes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bacteriocin Plasmids
  • Chromosomes, Bacterial
  • DNA Polymerase I / genetics
  • DNA Polymerase I / metabolism*
  • DNA-Directed DNA Polymerase / metabolism*
  • Escherichia coli / enzymology*
  • Escherichia coli / genetics
  • Genes, Bacterial
  • Methyl Methanesulfonate / pharmacology
  • Mutation
  • Thymine / metabolism
  • Transformation, Bacterial
  • Trimethoprim / pharmacology*
  • Ultraviolet Rays

Substances

  • Trimethoprim
  • Methyl Methanesulfonate
  • DNA Polymerase I
  • DNA-Directed DNA Polymerase
  • Thymine