THE RAD9 GENE CONTROLS THE CELL-CYCLE RESPONSE TO DNA DAMAGE IN SACCHAROMYCES-CEREVISIAE
THE RAD9 GENE CONTROLS THE CELL-CYCLE RESPONSE TO DNA DAMAGE IN SACCHAROMYCES-CEREVISIAE
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DOI：
10.1126/science.3291120
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发表时间：
1988-07-15
期刊：
影响因子：
56.9
通讯作者：
HARTWELL, LH
中科院分区：
文献类型：
--
作者：
WEINERT, TA;HARTWELL, LH
响应DNA损伤，在许多生物体中被捕细胞分裂。在酿酒酵母中，该反应的遗传基础的检查表明，RAD9基因产物对于阻止DNA损伤诱导的细胞分裂至关重要。野生型单倍体细胞在细胞周期的G2阶段被X射线停滞或延迟细胞分裂照射。在G2和死亡中，辐照G1和M期单倍体细胞在G2中不可逆转地停滞，而G2相位的G2相单倍体细胞延迟成正比，与恢复细胞分裂之前的损伤程度成正比。相反，在周期的任何阶段，受照射的RAD9细胞不会延迟G2中的细胞分裂，而是继续分裂几代并死亡。但是，如果用微管毒药处理在G2中阻断了辐照细胞在G2中封闭几个小时，则可以在辐照的RAD9细胞中进行有效的DNA修复。 RAD9依赖性反应检测到潜在的致命DNA损伤，并导致G2中的细胞停滞，直到修复了这种损伤。
Cell division is arrested in many organisms in response to DNA damage. Examinations of the genetic basis for this response in the yeast Saccharomyces cerevisiae indicate that the RAD9 gene product is essential for arrest of cell division induced by DNA damage. Wild-type haploid cell irradiated with x-rays either arrest or delay cell division in the G2 phase of the cell cycle. Irradiated G1 and M phase haploid cell arrest irreversibly in G2 and die, whereas irradiated G2 phase haploid cell delay in G2 for a time proportional to the extent of damage before resuming cell division. In contrast, irradiated rad9 cells in any phase of the cycle do not delay cell division in G2, but continue to divide for several generations and die. However, efficient DNA repair can occur in irradiated rad9 cells if irradiated cells are blocked for several hours in G2 by treatment with a microtubule poison. The RAD9-dependent response detects potentially lethal DNA damage and causes arrest of cells in G2 until such damage is repaired.