Cancer Research UK DNA Repair Enzymes Group, Genome Damage and Stability Centre, School of Life Sciences, University of Sussex, Brighton, United Kingdom.
Genome Damage and Stability Centre, School of Life Sciences, University of Sussex, Brighton, United Kingdom.
Elife. 2019 May 28;8:e44353. doi: 10.7554/eLife.44353.
Coordination of the cellular response to DNA damage is organised by multi-domain 'scaffold' proteins, including 53BP1 and TOPBP1, which recognise post-translational modifications such as phosphorylation, methylation and ubiquitylation on other proteins, and are themselves carriers of such regulatory signals. Here we show that the DNA damage checkpoint regulating S-phase entry is controlled by a phosphorylation-dependent interaction of 53BP1 and TOPBP1. BRCT domains of TOPBP1 selectively bind conserved phosphorylation sites in the N-terminus of 53BP1. Mutation of these sites does not affect formation of 53BP1 or ATM foci following DNA damage, but abolishes recruitment of TOPBP1, ATR and CHK1 to 53BP1 damage foci, abrogating cell cycle arrest and permitting progression into S-phase. TOPBP1 interaction with 53BP1 is structurally complimentary to its interaction with RAD9-RAD1-HUS1, allowing these damage recognition factors to bind simultaneously to the same TOPBP1 molecule and cooperate in ATR activation in the G1 DNA damage checkpoint.
细胞对 DNA 损伤的反应协调是由多结构域“支架”蛋白组织的,包括 53BP1 和 TOPBP1,它们可以识别其他蛋白质上的翻译后修饰,如磷酸化、甲基化和泛素化,并且本身就是这些调节信号的载体。在这里,我们表明,调节 S 期进入的 DNA 损伤检查点受 53BP1 和 TOPBP1 之间的磷酸化依赖性相互作用控制。TOPBP1 的 BRCT 结构域选择性地结合 53BP1 N 端的保守磷酸化位点。这些位点的突变不会影响 DNA 损伤后 53BP1 或 ATM 焦点的形成,但会消除 TOPBP1、ATR 和 CHK1 向 53BP1 损伤焦点的募集,从而阻止细胞周期停滞并允许进入 S 期。TOPBP1 与 53BP1 的相互作用与其与 RAD9-RAD1-HUS1 的相互作用在结构上是互补的,允许这些损伤识别因子同时结合到同一个 TOPBP1 分子上,并在 G1 DNA 损伤检查点中协同激活 ATR。