Repair and survival after UV in quiescent and proliferating Microtus agrestis cells: different rates of incision and different dependence on DNA precursor supply.
Cultured cells of Microtus agrestis, the common field vole, perform unscheduled DNA synthesis after UV irradiation. They respond to incubation with a DNA synthesis inhibitor (1-beta-D-arabinofuranosylcytosine) following UV in ways typical of cells capable of excision repair, with reduced survival and an accumulation of breaks in pre-existing DNA. Microtus cells irradiated with UV in a quiescent pre-S-phase state are more sensitive to UV than are proliferating cells, in terms of survival. Adding DNA precursors (deoxyribonucleosides), and--in case of proliferating cells--growing in complete rather than dialysed serum, enhance UV survival. Quiescent cells show a higher rate of endonucleolytic incision of DNA after UV than do proliferating cells. The balance between incision (producing single-strand DNA breaks) and repair DNA synthesis (leading to rejoining of breaks) is shifted by the addition of deoxyribonucleosides, which suggests that DNA precursor supply is a rate-limiting factor in repair. The lower survival of quiescent cells (in the absence of added deoxyribonucleosides) may be due to insufficient precursor supply to meet the demands of the high incision rate.
D000818:Animals; D003411:Arvicolinae; D001345:Autoradiography; D002453:Cell Cycle; D002460:Cell Line; D002470:Cell Survival; D002499:Centrifugation, Density Gradient; D004247:DNA / Q000528:radiation effects; D004260:DNA Repair; D004261:DNA Replication; D005260:Female; D007399:Interphase / Q000528:radiation effects; D011740:Pyrimidine Dimers / Q000378:metabolism; D014466:Ultraviolet Rays; D014740:Vidarabine / Q000494:pharmacology; D014965:X-Rays
D011740:Pyrimidine Dimers; D004247:DNA; D014740:Vidarabine