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保守的组蛋白变体H2A.Z揭示减数分裂重组起始。

The conserved histone variant H2A.Z illuminates meiotic recombination initiation.

作者信息

Yamada Shintaro, Kugou Kazuto, Ding Da-Qiao, Fujita Yurika, Hiraoka Yasushi, Murakami Hiroshi, Ohta Kunihiro, Yamada Takatomi

机构信息

Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Tokyo, 153-8902, Japan.

Memorial Sloan Kettering Cancer Center, New York, 10065, USA.

出版信息

Curr Genet. 2018 Oct;64(5):1015-1019. doi: 10.1007/s00294-018-0825-9. Epub 2018 Mar 16.

Abstract

Meiotic recombination ensures faithful chromosome segregation and confers genetic diversity to gametes, and thus, is a key DNA-templated reaction not only for sexual reproduction, but also evolution. This recombination is initiated by programmed DNA double strand breaks (DSBs), which are mainly formed at recombination hotspots. As meiotic DSB formation requires multiple proteins, it is regulated by chromatin structure. In particular, DSB occurs in a higher-order chromatin architecture termed "axis-loop", in which many loops protrude from proteinaceous axis. Previous studies have suggested that assembly of this structure is dependent on chromatin binding of cohesin, which in turn recruits proteins implicated in DSB formation. However, roles of chromatin in meiotic DSB formation are not fully characterized. This review article summarizes our recent report showing that the conserved histone H2A variant H2A.Z promotes meiotic DSB formation in fission yeast. Through a series of experiments, we found that, in H2A.Z-lacking mutants, multiple proteins involved in DSB formation, but not cohesin subunits, are less associated with chromatin. Strikingly, nuclei were more compact in the absence of H2A.Z. These observations led us to propose that fission yeast H2A.Z promotes meiotic DSB formation partly through modulating chromosome architecture to enhance interaction between DSB-related proteins and cohesin-loaded chromatin. In addition, biological implications of our findings are discussed, and their relevance to DSB formation in other species as well as to other DNA-related events are also provided.

摘要

减数分裂重组确保了染色体的忠实分离,并赋予配子遗传多样性,因此,它不仅是有性生殖,也是进化过程中关键的DNA模板反应。这种重组由程序性DNA双链断裂(DSB)引发,DSB主要在重组热点形成。由于减数分裂DSB的形成需要多种蛋白质,它受染色质结构调控。特别是,DSB发生在一种称为“轴-环”的高阶染色质结构中,其中许多环从蛋白质轴突出。先前的研究表明,这种结构的组装依赖于黏连蛋白与染色质的结合,而黏连蛋白反过来又招募参与DSB形成的蛋白质。然而,染色质在减数分裂DSB形成中的作用尚未完全明确。这篇综述文章总结了我们最近的报告,该报告表明保守的组蛋白H2A变体H2A.Z促进裂殖酵母中的减数分裂DSB形成。通过一系列实验,我们发现,在缺乏H2A.Z的突变体中,参与DSB形成的多种蛋白质,而非黏连蛋白亚基,与染色质的结合减少。令人惊讶的是,在没有H2A.Z的情况下,细胞核更加紧凑。这些观察结果使我们提出,裂殖酵母H2A.Z部分通过调节染色体结构来促进减数分裂DSB形成,以增强DSB相关蛋白与负载黏连蛋白的染色质之间的相互作用。此外,我们还讨论了研究结果的生物学意义,并提供了它们与其他物种中DSB形成以及其他DNA相关事件的相关性。

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