Villa-Hernández Sara, Bermejo Rodrigo
Centro de Investigaciones Biológicas (CIB-CSIC), Calle Ramiro de Maeztu 9, 28040, Madrid, Spain.
Wolfson Centre for Age-Related Diseases, King's College London, London, SE1 1UL, UK.
Curr Genet. 2018 Oct;64(5):1005-1013. doi: 10.1007/s00294-018-0824-x. Epub 2018 Mar 16.
Proliferating cells need to accurately duplicate and pass their genetic material on to daughter cells. Problems during replication and partition challenge the structural and numerical integrity of chromosomes. Diverse mechanisms, as the DNA replication checkpoint, survey the correct progression of replication and couple it with other cell cycle events to preserve genome integrity. The structural maintenance of chromosomes (SMC) cohesin complex primarily contributes to chromosome duplication by mediating the tethering of newly replicated sister chromatids, thus assisting their equal segregation in mitosis. In addition, cohesin exerts important functions in genome organization, gene expression and DNA repair. These are determined by cohesin's ability to bring together different DNA segments and, hence, by the fashion and dynamics of its interaction with chromatin. It recently emerged that cohesin contributes to the protection of stalled replication forks through a mechanism requiring its timely mobilization from unreplicated DNA and relocation to nascent strands. This mechanism relies on DNA replication checkpoint-dependent cohesin ubiquitylation and promotes nascent sister chromatid entrapment, likely contributing to preserve stalled replisome-fork architectural integrity. Here we review how cohesin dynamic association to chromatin is controlled through post-translational modifications to dictate its functions during chromosome duplication. We also discuss recent insights on the mechanism that mediates interfacing of replisome components with chromatin-bound cohesin and its contribution to the establishment of sister chromatid cohesion and the protection of stalled replication forks.
增殖细胞需要准确复制其遗传物质并将其传递给子细胞。复制和分配过程中的问题对染色体的结构和数量完整性构成挑战。多种机制,如DNA复制检查点,监测复制的正确进程,并将其与其他细胞周期事件相耦合,以维护基因组完整性。染色体结构维持(SMC)黏连蛋白复合体主要通过介导新复制的姐妹染色单体的拴系来促进染色体复制,从而协助它们在有丝分裂中均等分离。此外,黏连蛋白在基因组组织、基因表达和DNA修复中发挥重要作用。这些作用取决于黏连蛋白将不同DNA片段聚集在一起的能力,因此取决于其与染色质相互作用的方式和动态变化。最近发现,黏连蛋白通过一种需要其及时从未复制的DNA上转移并重新定位到新生链上的机制,来促进对停滞复制叉的保护。这种机制依赖于DNA复制检查点依赖性的黏连蛋白泛素化,并促进新生姐妹染色单体的捕获,这可能有助于维持停滞的复制体-叉的结构完整性。在这里,我们综述了黏连蛋白与染色质的动态结合是如何通过翻译后修饰来控制的,以决定其在染色体复制过程中的功能。我们还讨论了关于介导复制体成分与染色质结合的黏连蛋白相互作用的机制及其对姐妹染色单体黏连建立和停滞复制叉保护的贡献的最新见解。