Cell cycle-dependent regulation of excision repair of UV damage.
The incision step of excision repair of UV-damaged DNA, represented by the accumulation of DNA strand breaks in the presence of hydroxyurea and 1-beta-D-arabinofuranosylcytosine, was measured in cultured cells of Microtus agrestis during quiescence and at different times after release from quiescence. The UV dose-dependent kinetics of enzymic incision change rapidly through the first cell cycle after release, with a maximum potential for enzymic incision and a minimum affinity of the incision system for damage sites occurring in late G1. The potential for incision falls to a lower level as cells approach a randomly proliferating state, whilst the affinity rises. Incision activity declines rapidly after UV irradiation, leaving many damage sites unrepaired; the enhanced survival seen in cells held in quiescence after irradiation is thus partly due to some other repair mode.
D000818:Animals; D003411:Arvicolinae; D002453:Cell Cycle / Q000528:radiation effects*; D002470:Cell Survival; D002478:Cells, Cultured; D003561:Cytarabine / Q000494:pharmacology; D004260:DNA Repair / Q000528:radiation effects*; D004307:Dose-Response Relationship, Radiation; D006918:Hydroxyurea / Q000494:pharmacology; D007700:Kinetics; D014357:Trypsin / Q000494:pharmacology; D014466:Ultraviolet Rays
D003561:Cytarabine; D014357:Trypsin; D006918:Hydroxyurea