Abilities of wild-type and thymidine kinase-deficient Friend mouse erythroleukemia cells to undergo unscheduled DNA synthesis following mutagen treatment.
The abilities of wild-type and thymidine kinase-deficient Friend mouse erythroleukemia cells to perform unscheduled DNA synthesis (UDS), through the incorporation of [3H]deoxycytidine, were measured following damage with methyl methane sulfonate (MMS), ethyl methane sulfonate (EMS), and ultraviolet (UV) irradiation. For each mutagenic treatment, a positive and quantitatively similar response was observed for both wild-type and thymidine kinase-deficient cells. The extent of the response varied greatly, however, depending upon the mutagen used. The results contrast with the unscheduled incorporation of [3H]thymidine in wild-type cells following mutagen treatment, where less variation between the positive UDS responses elicited by MMS, EMS, and UV treatments was observed. Nevertheless, the results clearly indicate that thymidine kinase deficiency does not prevent excision repair (UDS) from occurring.
McKenna
P G
PG
McKelvey
V J
VJ
D000818:Animals; D002460:Cell Line; D004260:DNA Repair / Q000187:drug effects*; D005622:Friend murine leukemia virus; D004915:Leukemia, Erythroblastic, Acute / Q000201:enzymology / Q000235:genetics*; D007942:Leukemia, Experimental / Q000201:enzymology / Q000235:genetics*; D051379:Mice; D009152:Mutagenicity Tests; D009153:Mutagens; D009154:Mutation; D013937:Thymidine Kinase / Q000172:deficiency* / Q000235:genetics
D009153:Mutagens; D013937:Thymidine Kinase