染色质组装因子-1通过促进姐妹染色单体内聚来保持ctf4Δ细胞基因组的稳定性。

IF 4.1 Q2 CELL BIOLOGY
Nagham Ghaddar, Pierre Luciano, Vincent Géli, Yves Corda
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引用次数: 0

摘要

染色质组装和姐妹染色单体内聚的建立与DNA复制分叉的进展密切相关。在这里,我们研究了异三聚体染色质组装因子-1 (caf1)和核心复制体成分Ctf4之间的遗传相互作用,caf1是复制过程中染色质组装的核心成分。我们发现,在DNA复制过程中,ca -1缺陷细胞以及受新合成的H3-H4组蛋白沉积影响的细胞在ctf4Δ突变体中表现出严重的负生长。我们剖析了caf1在ctf4Δ酵母细胞中维持基因组稳定性中的作用。在缺乏CTF4的情况下,在经历复制问题的细胞中,在缺乏功能性s期检查点或功能性纺锤体检查点的细胞中,以及在缺乏涉及同源重组的DNA修复途径的细胞中,caf1对于细胞的生存至关重要。我们提供的证据表明,caf1以dna损伤依赖的方式影响染色质的内聚,并且在没有CTF4的情况下维持内聚是必不可少的。我们还发现eco1催化的Smc3乙酰化在没有caf1的情况下会减少。此外,我们描述了ca -1与参与黏结蛋白装载、黏结蛋白稳定和黏结蛋白成分的必要基因之间的遗传相互作用,表明当姐妹染色单体内聚受到影响时,ca -1对生存能力至关重要。最后,我们的数据表明,内聚所需的caf1依赖途径在功能上不同于Rtt101-Mms1-Mms22途径,后者在复制染色质组装中起作用。总的来说,我们的研究结果表明,在DNA复制过程中,新合成的H3-H4组蛋白的ca -1沉积创造了一个染色质环境,有利于姐妹染色单体的内聚和维持基因组的完整性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Chromatin assembly factor-1 preserves genome stability in <i>ctf4</i>Δ cells by promoting sister chromatid cohesion.

Chromatin assembly factor-1 preserves genome stability in <i>ctf4</i>Δ cells by promoting sister chromatid cohesion.

Chromatin assembly factor-1 preserves genome stability in <i>ctf4</i>Δ cells by promoting sister chromatid cohesion.

Chromatin assembly factor-1 preserves genome stability in ctf4Δ cells by promoting sister chromatid cohesion.

Chromatin assembly and the establishment of sister chromatid cohesion are intimately connected to the progression of DNA replication forks. Here we examined the genetic interaction between the heterotrimeric chromatin assembly factor-1 (CAF-1), a central component of chromatin assembly during replication, and the core replisome component Ctf4. We find that CAF-1 deficient cells as well as cells affected in newly-synthesized H3-H4 histones deposition during DNA replication exhibit a severe negative growth with ctf4Δ mutant. We dissected the role of CAF-1 in the maintenance of genome stability in ctf4Δ yeast cells. In the absence of CTF4, CAF-1 is essential for viability in cells experiencing replication problems, in cells lacking functional S-phase checkpoint or functional spindle checkpoint, and in cells lacking DNA repair pathways involving homologous recombination. We present evidence that CAF-1 affects cohesin association to chromatin in a DNA-damage-dependent manner and is essential to maintain cohesion in the absence of CTF4. We also show that Eco1-catalyzed Smc3 acetylation is reduced in absence of CAF-1. Furthermore, we describe genetic interactions between CAF-1 and essential genes involved in cohesin loading, cohesin stabilization, and cohesin component indicating that CAF-1 is crucial for viability when sister chromatid cohesion is affected. Finally, our data indicate that the CAF-1-dependent pathway required for cohesion is functionally distinct from the Rtt101-Mms1-Mms22 pathway which functions in replicated chromatin assembly. Collectively, our results suggest that the deposition by CAF-1 of newly-synthesized H3-H4 histones during DNA replication creates a chromatin environment that favors sister chromatid cohesion and maintains genome integrity.

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来源期刊
Cell Stress
Cell Stress Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (miscellaneous)
CiteScore
13.50
自引率
0.00%
发文量
21
审稿时长
15 weeks
期刊介绍: Cell Stress is an open-access, peer-reviewed journal that is dedicated to publishing highly relevant research in the field of cellular pathology. The journal focuses on advancing our understanding of the molecular, mechanistic, phenotypic, and other critical aspects that underpin cellular dysfunction and disease. It specifically aims to foster cell biology research that is applicable to a range of significant human diseases, including neurodegenerative disorders, myopathies, mitochondriopathies, infectious diseases, cancer, and pathological aging. The scope of Cell Stress is broad, welcoming submissions that represent a spectrum of research from fundamental to translational and clinical studies. The journal is a valuable resource for scientists, educators, and policymakers worldwide, as well as for any individual with an interest in cellular pathology. It serves as a platform for the dissemination of research findings that are instrumental in the investigation, classification, diagnosis, and therapeutic management of major diseases. By being open-access, Cell Stress ensures that its content is freely available to a global audience, thereby promoting international scientific collaboration and accelerating the exchange of knowledge within the research community.
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