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Activation of a DNA Damage Checkpoint Response in a TAF1-Defective Cell Line

机译：TAF1缺陷细胞系中DNA损伤检查点反应的激活。

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摘要

Although the link between transcription and DNA repair is well established, defects in the core transcriptional complex itself have not been shown to elicit a DNA damage response. Here we show that a cell line with a temperature-sensitive defect in TBP-associated factor 1 (TAF1), a component of the TFIID general transcription complex, exhibits hallmarks of an ATR-mediated DNA damage response. Upon inactivation of TAF1, ATR rapidly localized to subnuclear foci and contributed to the phosphorylation of several downstream targets, including p53 and Chk1, resulting in cell cycle arrest. The increase in p53 expression and the G1 phase arrest could be blocked by caffeine, an inhibitor of ATR. In addition, dominant negative forms of ATR but not ATM were able to override the arrest in G1. These results suggest that a defect in TAF1 can elicit a DNA damage response.
机译：尽管转录和DNA修复之间的联系已经建立，但核心转录复合物本身的缺陷尚未显示出引发DNA损伤反应的能力。在这里，我们显示了在TBP相关因子1（TAF1）（TFIID一般转录复合体的一个组成部分）中具有温度敏感缺陷的细胞系表现出ATR介导的DNA损伤反应的标志。 TAF1失活后，ATR迅速定位于亚核灶，并促进了多个下游靶标（包括p53和Chk1）的磷酸化，导致细胞周期停滞。咖啡因是ATR的抑制剂，可以阻止p53表达的增加和G 1 停滞。此外，ATR的显性阴性形式而非ATM能够克服G 1 中的逮捕。这些结果表明，TAF1中的缺陷可以引起DNA损伤反应。

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