Abstract
In mammalian cells, murine N-methylpurine DNA glycosylase (MPG) removes bases damaged spontaneously or by chemical agents through the process called base excision repair (BER). In this study, we investigated the influence of POL β deficiency on MPG-initiated BER efficiency and the expression levels of BER-related proteins in log-phase and growth-arrested (G(0)) mouse embryonic fibroblasts (MEFs). G(0) wild-type (WT) or POL β-deficient (Pol β-KO) cells showed greater resistance to methyl methanesulfonate than did log-phase cells, and repair of methylated bases was less efficient in the G(0) cells. Apex1 mRNA expression was significantly lower in Pol β-KO or G(0) WT MEFs than in log-phase WT MEFs. Moreover, although Mpg mRNA levels did not differ significantly among cell types, MPG protein levels were significantly higher in log-phase WT cells than in log-phase Pol β-KO cells or either type of G(0) cells. Additionally, proliferating cell nuclear antigen protein levels were also reduced in log-phase Pol β-KO cells or either type of G(0) cells. These results indicated that MPG-initiated BER functions mainly in proliferating cells, but less so in G(0) cells, and that POL β may be involved in regulation of the amount of intracellular repair proteins.