A novel checkpoint mechanism regulating the G1/S transition
A novel checkpoint mechanism regulating the G1/S transition
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DOI：
10.1101/gad.421807
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发表时间：
2007-03-15
影响因子：
10.5
通讯作者：
Boye, Erik
中科院分区：
文献类型：
--
作者：
Tvegard, Tonje;Soltani, Hela;Boye, Erik
G1 期裂殖酵母细胞的紫外线照射诱导复制起始因子染色质结合的延迟，并且一致地导致进入 S 期的短暂延迟。细胞周期延迟完全依赖于 Gcn2 激酶（一种营养状态传感器），并伴有翻译起始因子 eIF2 α 的磷酸化和翻译的普遍抑制。然而，DNA 复制所需因子的 G1 特异性合成并未因紫外线辐射而减少。细胞周期延迟代表了一个新的检查点，其具有不被电离辐射激活的新作用机制。
Ultraviolet irradiation of fission yeast cells in G1 phase induced a delay in chromatin binding of replication initiation factors and, consistently, a transient delay in S-phase entry. The cell cycle delay was totally dependent on the Gcn2 kinase, a sensor of the nutritional status, and was accompanied by phosphorylation of the translation initiation factor eIF2 alpha and by a general depression of translation. However, the G1-specific synthesis of factors required for DNA replication was not reduced by ultraviolet radiation. The cell cycle delay represents a novel checkpoint with a novel mechanism of action that is not activated by ionizing radiation.