DNA damage foci in mitosis are devoid of 53BP1
DNA damage foci in mitosis are devoid of 53BP1
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DOI：
10.4161/cc.8.20.9857
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发表时间：
2009-10-15
期刊：
影响因子：
4.3
通讯作者：
von Zglinicki, Thomas
中科院分区：
文献类型：
--
作者：
Nelson, Glyn;Buhmann, Matthias;von Zglinicki, Thomas
核DNA损伤灶是指正在进行的DNA损伤反应，是细胞周期停滞、细胞衰老和细胞凋亡的主要诱因。53BP1是DNA损伤反应的中心介质之一，也是DNA损伤活跃部位的组成部分。使用定量报告DNA损伤的AcGFP-53BP1c荧光融合蛋白，我们发现53BP1在G(2)/M时被抑制到含有Gamma H2A.X的DNA损伤灶中，这表明细胞通过抑制53BP1介导的DNA损伤信号继续通过G(2)检查点的Gamma H2A.X标记的双链断裂。
Nuclear DNA damage foci indicate ongoing DNA damage response, which is the major inducer of cell cycle arrest, cellular senescence and apoptosis. 53BP1 is one central mediator of the DNA damage response and a component of active DNA damage foci. Using an AcGFP-53BP1c fluorescent fusion protein that quantitatively reports DNA damage, we show that the recruitment of 53BP1 into gamma H2A.X-containing DNA damage foci was inhibited at G(2)/M. This suggests a possible mechanism for cells to continue through the G(2) checkpoint with gamma H2A.X-flagged double strand breaks via inhibition of 53BP1-mediated DNA damage signalling.