The lethal effects of uv and γ-rays were studied on synchronized cells of S. pombe with different defects in their repair pathways: UVS A cells do not excise pyrimidine dimers, UVS 1 cells are probably deficient in a repair mechanism related to recombination. <tex-math>${\rm UVS}^{+}$</tex-math> (wild-type) cells, after uv and γ-irradiation, /and UVS A cells after γ-irradiation, are the most resistant in the G2 phase of the mitotic cycle. These observations support the existence of a repair mechanism which acts on uv- and γ-induced lesions before DNA replication and is different from that of excision-resynthesis. After uv irradiation, it requires the participation of an incision enzyme also involved for excision repair. The uv response of UVS A cells is constant during the cycle, suggesting the presence of a repair mechanism acting during or after DNA replication. The uv resistance of UVS 1 cells decreases progressively from the beginning of the G2 to the end of the S period. This is interpreted in terms of delay available for excision repair. The practically constant response to uv of UVS A and of the double mutant UVS 1A, and to γ-rays of UVS 1A cells indicates that when variations occur, they are mainly due to differential repair abilities within the cycle.

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