Ultraviolet Light-Induced Division Delay in Synchronized Chinese Hamster Cells

Abstract

The age-dependent, ultraviolet light (UVL) (254 nm)-induced division delay of surviving and nonsurviving Chinese hamster cells was studied. The response was examined after UVL exposures adjusted to yield approximately the same survival levels at different stages of the cell cycle, 60% or 30% survival. Cells irradiated in the middle of S suffered the longest division delay, and cells exposed in mitosis or in G(1) had about the same smaller delay in division. Cells irradiated in G(2), however, were not delayed at either survival level. It was further established, after exposures that yielded about 30% survivors at various stages of the cycle, that surviving cells had shorter delays than nonsurvivors. This difference was not observed for cells in G(2) at the time of exposure; i.e., neither surviving nor nonsurviving G(2) cells were delayed in division. The examination of mitotic index vs. time revealed that most cells reach mitosis, but all of the increase in the number of cells in the population can be accounted for by the increase of the viable cell fraction. These observations suggest strongly that nonsurviving cells, although present during most of the experiment, are stopped at mitosis and do not divide. Cells in mitosis at the time of irradiation complete their division, and in the same length of time as unirradiated controls. Division and mitotic delays after UVL are relatively much larger than after X-ray doses that reduce survival to about the same level.

lncRNA-ZFAS1, an emerging gate-keeper in DNA damage-dependent transcriptional regulation

“…DNA damage checkpoints activated by severe stress can trigger permanent cellular outcomes such as apoptosis or senescence (Nyberg et al, 2002), meanwhile, failure to balance between cell cycle arrest and recovery can cause genome instability and impaired cell proliferation after DDR (Sogo et al, 2002). It has long been known that cells in different cell-cycle phases show drastic differences in survival under the same levels of ultraviolet light irradiation, which induces DNA adducts (Han et al, 1971). Although the molecular pathways of the DDR in each cell-cycle phase employ redundant mechanisms (Shaltiel et al, 2015), it has been proposed that each phase elicits distinct DNA checkpoint dynamics that link to the predicted cell-cycle outcomes (Chao et al, 2017).…”