Kilgas Susan, Swift Michelle L, Chowdhury Dipanjan
Division of Radiation and Genome Stability, Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Division of Radiation and Genome Stability, Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Department of Biological Chemistry & Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
DNA Repair (Amst). 2024 Dec;144:103779. doi: 10.1016/j.dnarep.2024.103779. Epub 2024 Oct 28.
53BP1 has several functions in the maintenance of genome integrity. It functions as a key mediator involved in double-strand break (DSB) repair, which functions to maintain a balance in the repair pathway choices and in preserving genomic stability. While its DSB repair functions are relatively well-characterized, its role in DNA replication and replication fork protection is less understood. In response to replication stress, 53BP1 contributes to fork protection by regulating fork reversal and restart. It helps maintain replication fork stability and speed, with 53BP1 loss leading to defective fork progression and increased sensitivity to replication stress agents. However, 53BP1's precise role in fork protection remains debated, as some studies have not observed protective effects. Therefore, it is critical to determine the role of 53BP1 in replication to better understand when it promotes replication fork protection, and the underlying mechanisms involved. Moreover, 53BP1's function in replication stress extends beyond its activity at active replication forks; it also forms specialized nuclear bodies (NBs) which protect stretches of under-replicated DNA (UR-DNA) transmitted from a previous cell cycle to daughter cells through mitosis. The mechanism of 53BP1 NBs in the coordination of replication and repair events at UR-DNA loci is not fully understood and warrants further investigation. The present review article focuses on elucidating 53BP1's functions in replication stress (RS), its role in replication fork protection, and the significance of 53BP1 NBs in this context to provide a more comprehensive understanding of its less well-established role in DNA replication.
53BP1在维持基因组完整性方面具有多种功能。它作为关键介质参与双链断裂(DSB)修复,该修复功能旨在维持修复途径选择的平衡并保持基因组稳定性。虽然其DSB修复功能相对已得到充分表征,但其在DNA复制和复制叉保护中的作用尚不太清楚。在应对复制应激时,53BP1通过调节复制叉逆转和重启来促进复制叉保护。它有助于维持复制叉的稳定性和速度,53BP1缺失会导致复制叉进展缺陷并增加对复制应激剂的敏感性。然而,53BP1在复制叉保护中的精确作用仍存在争议,因为一些研究未观察到保护作用。因此,确定53BP1在复制中的作用对于更好地理解其何时促进复制叉保护以及所涉及的潜在机制至关重要。此外,53BP1在复制应激中的功能不仅限于其在活跃复制叉处的活性;它还形成特殊的核体(NBs),这些核体保护通过有丝分裂从前一个细胞周期传递到子细胞的未复制DNA(UR-DNA)片段。53BP1核体在UR-DNA位点协调复制和修复事件的机制尚未完全了解,值得进一步研究。本综述文章重点阐述53BP1在复制应激(RS)中的功能、其在复制叉保护中的作用以及在此背景下53BP1核体的意义,以更全面地了解其在DNA复制中尚未完全明确的作用。