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A novel checkpoint mechanism regulating the G1/S transition.

机译:一种新的检查点机制,可调节G1 / S过渡。

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摘要

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 eIF2alpha 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.
机译:在G1期对裂变酵母细胞进行紫外线照射会导致复制起始因子的染色质结合延迟,并且始终如一地导致S期进入的短暂延迟。细胞周期延迟完全取决于营养状态的传感器Gcn2激酶,并伴有翻译起始因子eIF2alpha的磷酸化和翻译的普遍抑制。但是,DNA复制所需因子的G1特异性合成并未因紫外线而降低。细胞周期延迟代表了具有新颖作用机制的新颖检查点,而该作用机理并未被电离辐射激活。

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