Organ and cell specificity of base excision repair mutants in mice.
Genetically modified mouse models are a powerful approach to study the relation of a single gene-deletion to processes such as mutagenesis and carcinogenesis. The generation of base excision repair (BER) deficient mouse models has resulted in a re-examination of the cellular defence mechanisms that exist to counteract DNA base damage. This review discusses novel insights into the relation between specific gene-deletions and the organ and cell specificity of visible and molecular phenotypes, including accumulation of base lesions in genomic DNA and carcinogenesis. Although promising models exist, there is still a need for new models. These models should comprise combined deficiencies of DNA glycosylases which initiate the BER pathway, to elaborate on the repair redundancy, as well as conditional models of the intermediate steps of BER.
Larsen
Elisabeth
E
Centre for Molecular Biology and Neuroscience, Institute of Medical Microbiology, Rikshospitalet-Radiumhospitalet HF, 0027 Oslo, Norway. elisabel@medisin.uio.no
Meza
Trine J
TJ
Kleppa
Liv
L
Klungland
Arne
A
D000818:Animals; D004249:DNA Damage; D045647:DNA Glycosylases / Q000235:genetics / Q000378:metabolism; D004260:DNA Repair / Q000235:genetics*; D045643:DNA Repair Enzymes / Q000235:genetics / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D008957:Models, Genetic; D009154:Mutation; D009928:Organ Specificity
D045647:DNA Glycosylases; D045643:DNA Repair Enzymes