The Molecular Mechanism of Aurora-B Regulating Kinetochore-Microtubule Attachment in Mitosis and Oocyte Meiosis.

IF 1.7 4区 生物学 Q4 CELL BIOLOGY
Cytogenetic and Genome Research Pub Date : 2024-01-01 Epub Date: 2024-07-27 DOI:10.1159/000540588
Shanshan Chen, Qiqi Sun, Bo Yao, Yanping Ren
{"title":"The Molecular Mechanism of Aurora-B Regulating Kinetochore-Microtubule Attachment in Mitosis and Oocyte Meiosis.","authors":"Shanshan Chen, Qiqi Sun, Bo Yao, Yanping Ren","doi":"10.1159/000540588","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Aurora kinase B (Aurora-B), a member of the chromosomal passenger complex, is involved in correcting kinetochore-microtubule (KT-MT) attachment errors and regulating sister chromatid condensation and cytoplasmic division during mitosis.</p><p><strong>Summary: </strong>However, few reviews have discussed its mechanism in oocyte meiosis and the differences between its role in mitosis and meiosis. Therefore, in this review, we summarize the localization, recruitment, activation, and functions of Aurora-B in mitosis and oocyte meiosis. The accurate regulation of Aurora-B is essential for ensuring accurate chromosomal segregation and correct KT-MT attachments. Aurora-B regulates the stability of KT-MT attachments by competing with cyclin-dependent kinase 1 to control the phosphorylation of the SILK and RVSF motifs on kinetochore scaffold 1 and by competing with protein phosphatase 1 to influence the phosphorylation of NDC80 which is the substrate of Aurora-B. In addition, Aurora-B regulates the spindle assembly checkpoint by promoting the recruitment and activation of mitotic arrest deficient 2.</p><p><strong>Key messages: </strong>This review provides a theoretical foundation for elucidating the mechanism of cell division and understanding oocyte chromosomal aneuploidy.</p>","PeriodicalId":11206,"journal":{"name":"Cytogenetic and Genome Research","volume":null,"pages":null},"PeriodicalIF":1.7000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cytogenetic and Genome Research","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1159/000540588","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/7/27 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Aurora kinase B (Aurora-B), a member of the chromosomal passenger complex, is involved in correcting kinetochore-microtubule (KT-MT) attachment errors and regulating sister chromatid condensation and cytoplasmic division during mitosis.

Summary: However, few reviews have discussed its mechanism in oocyte meiosis and the differences between its role in mitosis and meiosis. Therefore, in this review, we summarize the localization, recruitment, activation, and functions of Aurora-B in mitosis and oocyte meiosis. The accurate regulation of Aurora-B is essential for ensuring accurate chromosomal segregation and correct KT-MT attachments. Aurora-B regulates the stability of KT-MT attachments by competing with cyclin-dependent kinase 1 to control the phosphorylation of the SILK and RVSF motifs on kinetochore scaffold 1 and by competing with protein phosphatase 1 to influence the phosphorylation of NDC80 which is the substrate of Aurora-B. In addition, Aurora-B regulates the spindle assembly checkpoint by promoting the recruitment and activation of mitotic arrest deficient 2.

Key messages: This review provides a theoretical foundation for elucidating the mechanism of cell division and understanding oocyte chromosomal aneuploidy.

Aurora-B 在有丝分裂和卵母细胞减数分裂中调控动点核-微管附着的分子机制
背景:极光激酶B(Aurora-B)是染色体客体复合体(CPC)的成员之一,在有丝分裂过程中参与纠正着丝点-微管(KT-MT)的附着错误并调节姐妹染色单体的凝集和细胞质的分裂。摘要:然而,很少有综述讨论其在卵母细胞减数分裂中的机制及其在有丝分裂和减数分裂中作用的差异。因此,本综述总结了Aurora-B在有丝分裂和卵母细胞减数分裂中的定位、招募、激活和功能。Aurora-B 的准确调控对确保染色体的准确分离和 KT-MT 的正确连接至关重要。Aurora-B 通过与细胞周期蛋白依赖性激酶 1(CDK1)竞争,控制动点支链支架 1 上的 SILK 和 RVSF 矩阵的磷酸化,以及与蛋白磷酸酶 1(PP1)竞争,影响 Aurora-B 底物 NDC80 的磷酸化,从而调节 KT-MT 连接的稳定性。此外,Aurora-B 还通过促进有丝分裂停滞缺陷 2(MAD2)的招募和激活来调节纺锤体组装检查点(SAC):本综述为阐明细胞分裂机制和理解卵母细胞染色体非整倍体提供了理论基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Cytogenetic and Genome Research
Cytogenetic and Genome Research 生物-细胞生物学
CiteScore
3.10
自引率
5.90%
发文量
25
审稿时长
1 months
期刊介绍: During the last decades, ''Cytogenetic and Genome Research'' has been the leading forum for original reports and reviews in human and animal cytogenetics, including molecular, clinical and comparative cytogenetics. In recent years, most of its papers have centered on genome research, including gene cloning and sequencing, gene mapping, gene regulation and expression, cancer genetics, comparative genetics, gene linkage and related areas. The journal also publishes key papers on chromosome aberrations in somatic, meiotic and malignant cells. Its scope has expanded to include studies on invertebrate and plant cytogenetics and genomics. Also featured are the vast majority of the reports of the International Workshops on Human Chromosome Mapping, the reports of international human and animal chromosome nomenclature committees, and proceedings of the American and European cytogenetic conferences and other events. In addition to regular issues, the journal has been publishing since 2002 a series of topical issues on a broad variety of themes from cytogenetic and genome research.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信