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DNA断裂的连接——DNA连接酶与聚(ADP-核糖)聚合酶之间的相互作用

Joining of DNA breaks- interplay between DNA ligases and poly (ADP-ribose) polymerases.

作者信息

Call Nicolas, Tomkinson Alan E

机构信息

University of New Mexico Comprehensive Cancer Center and the Departments of Internal Medicine, and Molecular Genetics & Microbiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico, USA.

University of New Mexico Comprehensive Cancer Center and the Departments of Internal Medicine, and Molecular Genetics & Microbiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico, USA.

出版信息

DNA Repair (Amst). 2025 May;149:103843. doi: 10.1016/j.dnarep.2025.103843. Epub 2025 May 2.

Abstract

The joining of DNA single- and double-strand breaks (SSB and DSB) is essential for maintaining genome stability and integrity. While this is ultimately accomplished in human cells by the DNA ligases encoded by the LIG1, LIG3 and LIG4 genes, these enzymes are recruited to DNA breaks through specific interactions with proteins involved in break sensing and recognition and/or break processing. In this review, we focus on the interplay between the DNA break-activated poly (ADP-ribose) polymerases, PARP1 and PARP2, poly (ADP-ribose) (PAR) and the DNA ligases in DNA replication and repair. The most extensively studied example of this interplay is the recruitment of DNA ligase IIIα (LigIIIα) and other repair proteins to SSBs through an interaction between XRCC1, a scaffold protein and partner protein of nuclear LigIIIα, and PAR synthesized by PARP1 and to a lesser extent PARP2. Recently, these proteins have been implicated in a back-up pathway for joining Okazaki fragments that appears to have a critical function even in cells with no defect in the major LigI-dependent pathway. Finally, we discuss the effects of FDA-approved PARP1/2 inhibitors on DNA replication and repair in cancer and non-malignant cells and the potential utility of DNA ligase inhibitors as cancer therapeutics.

摘要

DNA单链和双链断裂(SSB和DSB)的连接对于维持基因组稳定性和完整性至关重要。虽然这最终在人类细胞中由LIG1、LIG3和LIG4基因编码的DNA连接酶完成,但这些酶通过与参与断裂传感、识别和/或断裂处理的蛋白质的特异性相互作用被招募到DNA断裂处。在本综述中,我们聚焦于DNA断裂激活的聚(ADP - 核糖)聚合酶PARP1和PARP2、聚(ADP - 核糖)(PAR)与DNA连接酶在DNA复制和修复中的相互作用。这种相互作用最广泛研究的例子是通过支架蛋白XRCC1(核LigIIIα的伴侣蛋白)与PARP1合成的PAR(在较小程度上还有PARP2合成的PAR)之间的相互作用,将DNA连接酶IIIα(LigIIIα)和其他修复蛋白招募到SSB。最近,这些蛋白质参与了连接冈崎片段的备用途径,即使在主要的依赖LigI途径无缺陷的细胞中,该途径似乎也具有关键功能。最后,我们讨论了FDA批准的PARP1/2抑制剂对癌症和非恶性细胞中DNA复制和修复的影响以及DNA连接酶抑制剂作为癌症治疗药物的潜在效用。

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本文引用的文献

1
XRCC1 mediates PARP1- and PAR-dependent recruitment of PARP2 to DNA damage sites.
Nucleic Acids Res. 2025 Feb 8;53(4). doi: 10.1093/nar/gkaf086.
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Nucleic Acids Res. 2024 Sep 23;52(17):10341-10354. doi: 10.1093/nar/gkae672.
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Elife. 2024 Apr 5;12:RP89303. doi: 10.7554/eLife.89303.
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PARP1-DNA co-condensation drives DNA repair site assembly to prevent disjunction of broken DNA ends.
Cell. 2024 Feb 15;187(4):945-961.e18. doi: 10.1016/j.cell.2024.01.015. Epub 2024 Feb 5.

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