Repair of closely opposed cyclobutyl pyrimidine dimers in UV-sensitive human diploid fibroblasts.
An enzyme-sensitive site assay has been used to examine the fate of closely opposed pyrimidine dimers (bifilar enzyme-sensitive sites) in fibroblasts from individuals afflicted with various genetic disorders that confer increased cellular sensitivity to UV radiation. The disappearance of bifilar enzyme-sensitive sites was found to be normal in cells from individuals with Fanconi's anemia, Cockayne's syndrome, dyskeratosis congenita and the variant form of xeroderma pigmentosum. The rate of bifilar enzyme-sensitive site removal in XP cells assigned to complementation group C was reduced by an amount similar to that observed for the repair of isolated dimers. Our results indicate that the initiation of repair at closely opposed dimers is slow in XP-C cells but normal in all other cells examined.
D002460:Cell Line; D003057:Cockayne Syndrome / Q000235:genetics; D045647:DNA Glycosylases; D004260:DNA Repair; D005199:Fanconi Anemia / Q000235:genetics; D006801:Humans; D007642:Keratosis / Q000235:genetics*; D007700:Kinetics; D009699:N-Glycosyl Hydrolases; D011740:Pyrimidine Dimers / Q000378:metabolism*; D014466:Ultraviolet Rays; D014983:Xeroderma Pigmentosum / Q000235:genetics
D011740:Pyrimidine Dimers; D045647:DNA Glycosylases; D009699:N-Glycosyl Hydrolases