The DNA-binding protein CST associates with the cohesin complex and promotes chromosome cohesion.
The DNA-binding protein CST associates with the cohesin complex and promotes chromosome cohesion.
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DNA结合蛋白CST与粘着蛋白复合物结合并促进染色体的粘着。
DOI：
10.1016/j.jbc.2021.101026
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发表时间：
2021-09
期刊：
影响因子：
--
通讯作者：
Stewart JA
中科院分区：
文献类型：
--
作者：
Schuck PL;Ball LE;Stewart JA
姐妹染色单体内聚（SCC）是指在DNA复制后直到有丝分裂前姐妹染色单体之间的配对，是通过将内聚素复合物加载到新复制的染色单体上而建立的。然后必须维持粘着蛋白直到有丝分裂以防止分离缺陷和非整倍体。然而，SCC是如何建立和维持直到有丝分裂仍然不完全清楚，新出现的证据表明，复制应力可能导致过早的SCC损失。在这里，我们报告说，ssDNA结合蛋白CTC 1-STN 1-TEN 1（CST）在SCC的援助。CST主要在端粒长度调节中起作用，但也在复制重启和DNA修复中起作用。在CST亚基耗尽后，我们观察到SCC完全丧失的增加。此外，我们确定CST与cohesin复合物相关。出乎意料的是，我们没有发现证据的改变cohesin加载或有丝分裂进展的情况下，CST，然而，我们确实发现，各种复制抑制剂的治疗增加了CST和cohesin之间的关联。由于复制应激最近被证明会诱导SCC损失，因此我们假设可能需要CST来维持或重塑DNA复制叉停滞后的SCC。与此观点一致，外源性复制应激后，CST耗尽的细胞中SCC损失大大增加。根据我们的研究结果，我们建议，CST艾滋病在维护SCC停滞复制叉，以防止过早的凝聚力损失。
Sister chromatid cohesion (SCC), the pairing of sister chromatids after DNA replication until mitosis, is established by loading of the cohesin complex on newly replicated chromatids. Cohesin must then be maintained until mitosis to prevent segregation defects and aneuploidy. However, how SCC is established and maintained until mitosis remains incompletely understood, and emerging evidence suggests that replication stress may lead to premature SCC loss. Here, we report that the ssDNA-binding protein CTC1-STN1-TEN1 (CST) aids in SCC. CST primarily functions in telomere length regulation but also has known roles in replication restart and DNA repair. After depletion of CST subunits, we observed an increase in the complete loss of SCC. In addition, we determined that CST associates with the cohesin complex. Unexpectedly, we did not find evidence of altered cohesin loading or mitotic progression in the absence of CST; however, we did find that treatment with various replication inhibitors increased the association between CST and cohesin. Because replication stress was recently shown to induce SCC loss, we hypothesized that CST may be required to maintain or remodel SCC after DNA replication fork stalling. In agreement with this idea, SCC loss was greatly increased in CST-depleted cells after exogenous replication stress. Based on our findings, we propose that CST aids in the maintenance of SCC at stalled replication forks to prevent premature cohesion loss.
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影响因子：
4
作者：
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影响因子：
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发表时间：
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期刊：
Current biology : CB
影响因子：
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作者：
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通讯作者：
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影响因子：
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作者：
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