title: Abundance of BER-related proteins depends on cell proliferation status and the presence of DNA polymerase β.
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.
authors.affiliation: Department of Advanced Pathobiology, Graduate School of Life and Environmental Sciences, Osaka Prefecture University, 1-58 Rinku Ourai-Kita, Izumisano, Osaka 598-8531, Japan.
authors.forename: Mizuki
authors.initials: M
authors.lastname: Yamamoto
authors.affiliation: Department of Advanced Pathobiology, Graduate School of Life and Environmental Sciences, Osaka Prefecture University, 1-58 Rinku Ourai-Kita, Izumisano, Osaka 598-8531, Japan yamamoto@vet.osakafu-u.ac.jp.
authors.forename: Ryohei
authors.initials: R
authors.lastname: Yamamoto
authors.affiliation: Department of Structural and Functional Biosciences for Animals, Graduate School of Life and Environmental Sciences, Osaka Prefecture University, 1-58 Rinku Ourai-Kita, Izumisano, Osaka 598-8531, Japan.
authors.forename: Shigeo
authors.initials: S
authors.lastname: Takenaka
authors.affiliation: Department of Advanced Pathobiology, Graduate School of Life and Environmental Sciences, Osaka Prefecture University, 1-58 Rinku Ourai-Kita, Izumisano, Osaka 598-8531, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Matsuyama
authors.affiliation: Department of Advanced Pathobiology, Graduate School of Life and Environmental Sciences, Osaka Prefecture University, 1-58 Rinku Ourai-Kita, Izumisano, Osaka 598-8531, Japan.
authors.forename: Kihei
authors.initials: K
authors.lastname: Kubo
mesh_terms: D000818:Animals; D002453:Cell Cycle / Q000502:physiology*; D049109:Cell Proliferation / Q000502:physiology; D002478:Cells, Cultured; D045647:DNA Glycosylases / Q000378:metabolism; D019951:DNA Polymerase beta / Q000378:metabolism*; D004260:DNA Repair / Q000502:physiology*; D004268:DNA-Binding Proteins / Q000378:metabolism*; D005347:Fibroblasts / Q000166:cytology* / Q000502:physiology*; D018507:Gene Expression Regulation, Developmental / Q000502:physiology; D051379:Mice
chemical_list: D004268:DNA-Binding Proteins; D019951:DNA Polymerase beta; D045647:DNA Glycosylases
keywords: BER; MPG; POL β; cell proliferation; mouse
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