DNA repair in an active gene: removal of pyrimidine dimers from the DHFR gene of CHO cells is much more efficient than in the genome overall.
DNA repair was measured in the dihydrofolate reductase gene in Chinese hamster ovary cells, amplified for the gene, by quantitating pyrimidine dimers with a specific UV-endonuclease. More than two thirds of the dimers had been removed from a 14.1 kb restriction fragment of the gene by 26 hr after irradiation (20 J/m2), while little removal was detected in fragments upstream of the gene and only 15% were removed from the genome overall. This suggests that damage processing can vary according to function or activity of affected sequences, which has general implications for correlations of DNA repair with survival and mutagenesis. Perhaps preferential repair of vital sequences facilitates UV-resistance of these cells despite low overall repair levels.
D000818:Animals; D001483:Base Sequence; D002460:Cell Line; D002470:Cell Survival / Q000528:radiation effects; D006224:Cricetinae; D003412:Cricetulus; D004260:DNA Repair; D004706:Endodeoxyribonucleases; D005260:Female; D009097:Multienzyme Complexes; D009699:N-Glycosyl Hydrolases; D011740:Pyrimidine Dimers / Q000032:analysis*; D013762:Tetrahydrofolate Dehydrogenase / Q000235:genetics*
D009097:Multienzyme Complexes; D011740:Pyrimidine Dimers; C032219:UV endonuclease; D013762:Tetrahydrofolate Dehydrogenase; D004706:Endodeoxyribonucleases; D009699:N-Glycosyl Hydrolases