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Base excision repair deficient mice lacking the Aag alkyladenine DNA glycosylase.

3-methyladenine (3MeA) DNA glycosylases remove 3MeAs from alkylated DNA to initiate the base excision repair pathway. Here we report the generation of mice deficient in the 3MeA DNA glycosylase encoded by the Aag (Mpg) gene. Alkyladenine DNA glycosylase turns out to be the major DNA glycosylase not only for the cytotoxic 3MeA DNA lesion, but also for the mutagenic 1,N6-ethenoadenine (epsilonA) and hypoxanthine lesions. Aag appears to be the only 3MeA and hypoxanthine DNA glycosylase in liver, testes, kidney, and lung, and the only epsilonA DNA glycosylase in liver, testes, and kidney; another epsilonA DNA glycosylase may be expressed in lung. Although alkyladenine DNA glycosylase has the capacity to remove 8-oxoguanine DNA lesions, it does not appear to be the major glycosylase for 8-oxoguanine repair. Fibroblasts derived from Aag -/- mice are alkylation sensitive, indicating that Aag -/- mice may be similarly sensitive.

Pubmed ID: 9371804


  • Engelward BP
  • Weeda G
  • Wyatt MD
  • Broekhof JL
  • de Wit J
  • Donker I
  • Allan JM
  • Gold B
  • Hoeijmakers JH
  • Samson LD


Proceedings of the National Academy of Sciences of the United States of America

Publication Data

November 25, 1997

Associated Grants

  • Agency: NCI NIH HHS, Id: 5T32CA09078
  • Agency: NIEHS NIH HHS, Id: P01-ES03926
  • Agency: NCI NIH HHS, Id: R01 CA055042
  • Agency: NCI NIH HHS, Id: R01 CA55042

Mesh Terms

  • Alkylating Agents
  • Animals
  • Crosses, Genetic
  • DNA Glycosylases
  • DNA Repair
  • DNA, Complementary
  • Female
  • Genotype
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • N-Glycosyl Hydrolases