Trimethoprim-induced DNA polymerase I deficiency in Escherichia coli K-12.
AUTOR(ES)
Mukhopadhyay, P
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=217579Documentos Relacionados
- Bacteriophage Mu-1-induced permeability mutants in Escherichia coli K-12.
- Spontaneous and UV-induced mutations in Escherichia coli K-12 strains with altered or absent DNA polymerase I.
- Hfr formation by I pilus-determining plasmids in Escherichia coli K-12.
- Cadmium uptake in Escherichia coli K-12.
- Uracil-DNA glycosylase causes 5-bromodeoxyuridine photosensitization in Escherichia coli K-12.