Ultraviolet (UV) radiation is a major environmental mutagen. Exposure to UV leads to a sharp peak of γH2AX, the phosphorylated form of the histone variant H2AX, in the S phase within an asynchronous population of cells. γH2AX is often considered a definitive marker of DNA damage inside a cell. In this report, we show that γH2AX in the S-phase cells after UV irradiation reports neither on the extent of primary DNA damage in the form of cyclobutane pyrimidine dimers nor on the extent of its secondary manifestations in the form of DNA double-strand breaks or in the inhibition of global transcription. Instead, γH2AX in the S phase corresponds to the sites of active replication at the time of UV irradiation. This accumulation of γH2AX at replication sites slows down the replication. However, the cells do complete the replication of their genomes and arrest within the G₂ phase. Our study suggests that it is not DNA damage, but the response elicited, which peaks in the S phase upon UV irradiation.

中文翻译：

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紫外线照射后处于S期的γH2AX对应于DNA复制，并且没有报告DNA损伤的程度。

紫外线（UV）辐射是主要的环境诱变剂。暴露于紫外线会导致异步细胞群体中S期的γH2AX（组蛋白变体H2AX的磷酸化形式）的尖峰。γH2AX通常被认为是细胞内DNA损伤的确定标记。在本报告中，我们表明，紫外线照射后S期细胞中的γH2AX既没有报告以环丁烷嘧啶二聚体形式发生的初级DNA损伤的程度，也没有以DNA双链断裂的形式报告其次要表现的程度或抑制全局转录。相反，在S相中的γH2AX对应于紫外线照射时的活性复制位点。γH2AX在复制位点的这种积累会减慢复制速度。然而，₂阶段。我们的研究表明，不是DNA损伤，而是引起了反应，该反应在紫外线照射下在S期达到峰值。