Excision-repair in primary cultures of mouse embryo cells and its decline in progressive passages and established cell lines.
Fibroblasts of mouse embryo cells from early subcultures excise pyrimidine dimers to an extent and at a rate comparable to those observed in human cells. The only apparent difference is that in primary mouse cells dimers are excised in an acid-insoluble form. Dimer excision in mouse embryo fibroblasts declines abruptly after the fourth to the sixth subculture and is not detectable in the permanent cell line 3T3. It is suggested that cessation of excision-repair may be due to genetic repression.
D000818:Animals; D001665:Binding Sites; D002460:Cell Line; D002467:Cell Nucleus / Q000378:metabolism / Q000528:radiation effects; D004260:DNA Repair; D004307:Dose-Response Relationship, Radiation; D004622:Embryo, Mammalian; D005347:Fibroblasts / Q000378:metabolism / Q000528:radiation effects; D051379:Mice; D011742:Pyrimidine Nucleotides / Q000378:metabolism; D011830:Radiation Effects
D011742:Pyrimidine Nucleotides