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预 RC 蛋白 MCM7 耗竭通过抑制 CDK1 活性促进有丝分裂退出。

Pre-RC Protein MCM7 depletion promotes mitotic exit by Inhibiting CDK1 activity.

机构信息

Institute of Biotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.

Department of Endoscopy, Sun Yat-sen University Cancer Center, Guangzhou, China.

出版信息

Sci Rep. 2017 Jun 6;7(1):2854. doi: 10.1038/s41598-017-03148-3.

DOI:10.1038/s41598-017-03148-3
PMID:28588300
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5460140/
Abstract

MCM7, a subunit of mini-chromosome maintenance proteins (MCM) complex, plays an important role in initiating DNA replication during the G1 phase and extending DNA strands during the S phase. Here, we demonstrated that MCM7 is not only sustained but maintains association with chromatin during M phase. Remarkably, MCM7 siRNA can accelerate mitotic exit. MCM7 depletion leads to CDK1 inactivation and promotes subsequent cohesin/RAD21 cleavage, which eventually leads to sister chromatin segregation. Moreover, MCM7 is co-localized with tubulin in the mitotic cells and MCM7 depletion results in aberrant mitosis. Our results indicate that MCM7 may exert certain functions on spindle formation to prevent cytokinesis during early mitosis by regulating CDK1 activity.

摘要

MCM7 是微染色体维持蛋白(MCM)复合物的一个亚基,在 G1 期启动 DNA 复制和 S 期延伸 DNA 链的过程中发挥重要作用。在这里,我们证明 MCM7 在有丝分裂期间不仅持续存在,而且还与染色质保持关联。值得注意的是,MCM7 siRNA 可以加速有丝分裂退出。MCM7 耗竭导致 CDK1 失活,并促进随后的黏连蛋白/RAD21 切割,最终导致姐妹染色单体分离。此外,MCM7 在有丝分裂细胞中与微管蛋白共定位,MCM7 耗竭导致有丝分裂异常。我们的结果表明,MCM7 可能通过调节 CDK1 活性在纺锤体形成中发挥某些功能,以防止早期有丝分裂中的胞质分裂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3993/5460140/542dc0740823/41598_2017_3148_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3993/5460140/aa4bc252b163/41598_2017_3148_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3993/5460140/6f864a8ad0ec/41598_2017_3148_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3993/5460140/0dd32dd26b40/41598_2017_3148_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3993/5460140/55a10b45cf36/41598_2017_3148_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3993/5460140/a3270f230944/41598_2017_3148_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3993/5460140/542dc0740823/41598_2017_3148_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3993/5460140/aa4bc252b163/41598_2017_3148_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3993/5460140/6f864a8ad0ec/41598_2017_3148_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3993/5460140/0dd32dd26b40/41598_2017_3148_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3993/5460140/55a10b45cf36/41598_2017_3148_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3993/5460140/a3270f230944/41598_2017_3148_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3993/5460140/542dc0740823/41598_2017_3148_Fig6_HTML.jpg

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