METHYLADENINE DNA GLYCOSYLASE, MDG| 3-@METHYLADENINE DNA GLYCOSYLASE| 3@MeAde DNA GLYCOSYLASE| 3-@ALKYLADENINE DNA GLYCOSYLASE, AAG| ALKYLPURINE DNA N-GLYCOSYLASE, APNG|
The bacterial enzyme 3-methyladenine (3MeA) DNA glycosylase repairs the lethal lesion 3MeA that blocks DNA
replication in Escherichia coli. The removal of 3MeA is mediated by two 3MeA DNA glycosylases in E. coli, encoded by
the alkA and tag genes.
General function
Cell death/survival, DNA Replication, Enzyme, Transferase
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Cellular localization
Nuclear
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Ovarian function
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Kim NK, et al 2000 reported spatial expression of a DNA repair gene, N-methylpurine-DNA
glycosylase (MPG) during development in mice.
MPG mRNA expression was revealed at
various stages of mouse development from day 7.5 p.c. (post coitum) embryo to day
400 mature adult by Northern blot hybridization or RT-PCR. MPG
transcripts were abundant in the mouse embryo during pregnancy and in adult testis and
ovary. These data suggest that an elevated rate of MPG transcription is required
for DNA replication.
Expression regulated by
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Ovarian localization
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Kim NK, et al 2002 reported that, in a normal ovary, immunostaining for MPG was observed in the nucleus of oocyte, granulosa and stromal cells. MPG was stained mostly in the nucleus and faintly-stained in the cytoplasm of normal coelomic epithelium as well as in benign epithelial ovarian tumors. However, the MPG expression, of the nucleus in malignant epithelial tumors, both serous and mucinous type, disappeared. The subcellular localization of MPG in the tissues tested was heterogeneous, while the altered MPG expression was found in ovarian tumor and spermatogenic arrest testis. These results suggest MPGs role in human gonadal tissues and raise the possibility that the altered mRNA level and intracellular localization could be associated with ovarian tumorigenesis and male infertility.
Follicle stages
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Phenotypes
Mutations
1 mutations
Species: mouse
Mutation name: None
type: null mutation fertility: fertile Comment: [Elder et al. (1998)$ 9742100] developed mice deficient in alkylpurine-DNA-N-glycosylase by targeted disruption. Following
treatment with DNA-methylating agents, increased persistence of 7-methylguanine (meG) was found in liver sections of
APNG knockout mice in comparison with wildtype mice, demonstrating an in vivo phenotype for the APNG-null
animals. Unlike other null mutants of the basic excision repair pathway, the APNG knockout mice exhibited a very mild
phenotype, showed no outward abnormalities, were fertile, and had an apparently normal lifespan.