Altered induction of the adaptive response to alkylation damage in Escherichia coli recF mutants.
AUTOR(ES)
Volkert, M R
RESUMO
Escherichia coli recF mutants are hypermutable when treated with methyl methanesulfonate (G. C. Walker, Mol. Gen. Genet. 152:93-103, 1977). In this study, methylation hypermutability of recF mutant strains was examined, and it was found that recF+ is required for normal induction of the adaptive response to alkylation damage. Although this regulatory effect of recF mutations results in reduced levels of enzymes that specifically repair methyl lesions in DNA, it only partially explains the hypermutability. Further examination showed that methylation hypermutability of recF mutant strains required a functional umuDC operon, a component of the SOS response. These results lead to the hypothesis that methylation hypermutability results from the effects of recF mutations on the induction of both the SOS response and the adaptive response.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=209560Documentos Relacionados
- Regulatory role of recF in the SOS response of Escherichia coli: impaired induction of SOS genes by UV irradiation and nalidixic acid in a recF mutant.
- Molecular analysis of the recF gene of Escherichia coli.
- RecOR suppression of recF mutant phenotypes in Escherichia coli K-12.
- Induction of Colicin E1 Synthesis in Recombination-Defective Mutants in Both the RecBC and RecF Pathways
- Suppression of the UV-sensitive phenotype of Escherichia coli recF mutants by recA(Srf) and recA(Tif) mutations requires recJ+.