Mutations associated with base excision repair deficiency and methylation-induced genotoxic stress.

ABSTRACT: The long-term effect of exposure to DNA alkylating agents is entwined with the cell's genetic capacity for DNA repair and appropriate DNA damage responses. A unique combination of environmental exposure and deficiency in these responses can lead to genomic instability; this "gene-environment interaction" paradigm is a theme for research on chronic disease etiology. In the present study, we used mouse embryonic fibroblasts with a gene deletion in the base excision repair (BER) enzymes DNA beta-polymerase (beta-pol) and alkyladenine DNA glycosylase (AAG), along with exposure to methyl methanesulfonate (MMS) to study mutagenesis as a function of a particular gene-environment interaction. The beta-pol null cells, defective in BER, exhibit a modest increase in spontaneous mutagenesis compared w

SUBMITTER: Sobol RW 

PROVIDER: S-EPMC124494 | biostudies-literature | 2002 May

REPOSITORIES: biostudies-literature