作者: A. J. Callegari , T. J. Kelly
关键词: CHEK1 、 G2-M DNA damage checkpoint 、 Cell cycle 、 Postreplication repair 、 Molecular biology 、 DNA damage 、 Nucleotide excision repair 、 Biology 、 DNA replication 、 DNA repair
摘要: Eukaryotic cells irradiated with high doses of UV exhibit cell-cycle responses referred to as G1/S, intraS, and G2/M checkpoints. After a moderate dose that approximates sunlight exposure is lethal fission yeast checkpoint mutants, we found unexpectedly these do not occur. Instead, at all stages the cell cycle carry lesions into S phase delay progression for hours after completion bulk DNA synthesis. Both replication kinase, Chk1, are required generate this response. UV-irradiation Δchk1 causes chromosome damage loss viability only have replicated entered mitosis. These data suggest an important physiological role response provide time postreplication repair.