Recovery from post-irradiation inhibition of DNA synthesis in an ultraviolet-sensitive mutant mouse cell

Abstract

Mouse cells in culture are inefficient in excision of pyrimidine dimers induced by ultraviolet irradiation (UV) (Lehmann and Kirk-Bell, 1972). Despite this inefficiency, mouse cells are as resistant to the lethal effects of UV as are excisionproficient human cells (Rauth et al., 1974; Sato and Setlow, 1981). The mechanism of tolerance by which mouse cells survive UV irradiation is not clear. UV-sensitive mouse cell mutants, if isolated, would be useful for the study of this mechanism. We have isolated a UV-sensitive mutant, Q31, from mouse lymphoma L5178Y cells (Sato and Hieda, 1979), and this mutant has been examined for excision and postreplication repairs of UV damage (Sato and Setlow, 1981). The results show that the parental mouse cells remove 10-20% of induced dimers during the 24-h incubation period and that Q31 cells cannot remove detectable amounts of dimers. Hence the lack of excision repair may be to some extent responsible for the elevated UV sensitivity in mutant cells. Post-replication repair, which will represent another tolerance mechanism operative in mouse cells, was examined to find out whether this mechanism is missing from mutant Q31 cells; the increase in molecular weights of newly synthesized DNA after irradiation was compared between mutant and parental cells, The size of DNA synthesized immediately after irradiation was smaller in mutant than in parental cells, but the rate of DNA-chain elongation was not much different between mutant and parental cells (Sato and Setlow, 1981). However, the changes in the rates of DNA synthesis during the post-irradiation incubation period have not been determined yet. For this report we measured the rates of DNA synthesis after irradiation and observed an affected recovery of UV-inhibited DNA synthesis in mutant cells.