Ultraviolet light induction of diphtheria toxin-resistant mutations in normal and DNA repair-deficient human and Chinese hamster fibroblasts.
The role of unrepaired DNA lesions in the production of mutations is suspected of contributing to the initiation phase of carcinogenesis. Since the molecular basis of mutagenesis is not understood in eukaryotic cells, development of new genetic markers for quantitative in vitro measurement of mutations for mammalian cells is needed. Furthermore, mammalian cells, genetically deficient for various DNA repair enzymes, will be needed to study the role of unrepaired DNA lesions in mutagenesis. The results in this report relate to preliminary attempts (1) to characterize the diphtheria toxin resistance marker as a useful quantitative genetic marker in human cells and (2) to isolate and characterize various DNA repair-deficient Chinese hamster cells.
D000818:Animals; D001973:Bromodeoxyuridine / Q000494:pharmacology; D002470:Cell Survival / Q000187:drug effects / Q000528:radiation effects; D002999:Clone Cells; D006224:Cricetinae; D003412:Cricetulus; D004260:DNA Repair; D004167:Diphtheria Toxin / Q000494:pharmacology*; D004307:Dose-Response Relationship, Radiation; D004351:Drug Resistance; D005347:Fibroblasts / Q000187:drug effects / Q000528:radiation effects*; D006801:Humans; D009154:Mutation; D014466:Ultraviolet Rays; D014983:Xeroderma Pigmentosum / Q000235:genetics
D004167:Diphtheria Toxin; D001973:Bromodeoxyuridine