对NuA4/TIP60介导的DNA修复途径选择的新见解。
New insights into the DNA repair pathway choice with NuA4/TIP60.
作者信息
Lashgari Anahita, Kougnassoukou Tchara Pata-Eting, Lambert Jean-Philippe, Côté Jacques
机构信息
St-Patrick Research Group in Basic Oncology, Canada; Laval University Cancer Research Center, CHU de Québec-Université Laval Research Center, Quebec City, QC, Canada; Department of Molecular Medicine, Big Data Research Center, Université Laval, Quebec, Canada.
Laval University Cancer Research Center, CHU de Québec-Université Laval Research Center, Quebec City, QC, Canada; Department of Molecular Medicine, Big Data Research Center, Université Laval, Quebec, Canada.
出版信息
DNA Repair (Amst). 2022 May;113:103315. doi: 10.1016/j.dnarep.2022.103315. Epub 2022 Mar 3.
In eukaryotic cells, DNA double-strand breaks (DSBs) can be repaired through two main pathways, non-homologous end-joining (NHEJ) or homologous recombination (HR). The selection of the repair pathway choice is governed by an antagonistic relationship between repair factors specific to each pathway, in a cell cycle-dependent manner. The molecular mechanisms of this decision implicate post-translational modifications of chromatin surrounding the break. Here, we discuss the recent advances regarding the function of the NuA4/TIP60 histone acetyltransferase/chromatin remodeling complex during DSBs repair. In particular, we emphasise the contribution of NuA4/TIP60 in repair pathway choice, in collaboration with the SAGA acetyltransferase complex, and how they regulate chromatin dynamics, modify non-histone substrates to allow DNA end resection and recombination.
在真核细胞中，DNA双链断裂（DSB）可通过两条主要途径进行修复，即非同源末端连接（NHEJ）或同源重组（HR）。修复途径的选择由每个途径特有的修复因子之间的拮抗关系决定，且依赖于细胞周期。这一决定的分子机制涉及断裂周围染色质的翻译后修饰。在此，我们讨论了关于NuA4/TIP60组蛋白乙酰转移酶/染色质重塑复合物在DSB修复过程中功能的最新进展。特别强调了NuA4/TIP60与SAGA乙酰转移酶复合物协同作用在修复途径选择中的贡献，以及它们如何调节染色质动态变化、修饰非组蛋白底物以促进DNA末端切除和重组。
Zotero 插件