期刊文献+

酵母有丝分裂染色体异常分离机制 被引量:1

Mechanism of Abnormal Chromosomal Segregation in Yeast Mitosis
下载PDF
导出
摘要 有丝分裂是真核生物细胞遗传和增殖发育的基础,主要分为S期和M期,其中M期是细胞分裂和遗传物质传递的重要过程。染色体的正确分离受到多种细胞机制的高度调控,是保证子代细胞遗传信息完整性的关键。本文主要以典型的真核生物酵母细胞为研究模型,综述了酵母在有丝分裂过程中染色体分离异常形成非整倍体的具体机制。分别包括纺锤体组装监控机制失效、姐妹染色单体黏结蛋白缺陷、动粒-纺锤体微管结合错误和多中心体途径4个方面。并讨论了非整倍体现象对酵母细胞造成的影响,以期更好的理解非整倍体酵母的生理及遗传特性。 Mitosis is the basis of cell genetics,proliferation and development in eukaryotes.It is mainly divided into S phase and M phase,of which M phase is an important process of cell division and transmission of genetic material.The correct segregation of chromosome is highly regulated by a variety of cellular mechanisms,and is the key to ensuring the integrity of the genetic information of the offspring cells.This article mainly uses typical eukaryotic yeast cells as the research model,and reviews the specific mechanisms of abnormal chromosome segregation and aneuploidy formation in the yeast during mitosis.There are four aspects including failure of spindle assembly monitoring mechanism,sister chromatid adhesion protein defect,kinetochore-spindle microtubule binding error,and polycentric pathway.The effects of aneuploidy on the yeast cells are also discussed,aiming to better understand the physiological and genetic characteristics of aneuploidy yeast.
作者 魏文青 谢泽雄 WEI Wen-qing;XIE Ze-xiong(Frontier Science Center for Synthetic Biology,Key Laboratory of System Bioengineering(Ministry of Education),School of Chemical Engineering and Technology,Tianjin University,Tianjin 300072)
出处 《生物技术通报》 CAS CSCD 北大核心 2021年第12期227-234,共8页 Biotechnology Bulletin
基金 国家自然科学基金创新研究群体项目(21621004)。
关键词 酵母 非整倍体 染色体异常分离 有丝分裂 yeast aneuploidy abnormal chromosome segregation mitosis
  • 相关文献

参考文献3

二级参考文献93

  • 1王应雄,刘学庆,翁亚光,何俊琳,郑增淳.HeLa 细胞染色体着丝粒点变异研究[J].肿瘤,1997,17(3):151-153. 被引量:5
  • 2Stanford J S, Lieberman S L, Wong V L, et al. Regulation of the G2/M transition in oocytes of Xenopus tropicalis. Dev Biol, 2003, 260(2): 438-448.
  • 3Mendez R, Hake L E, Andresson T, et al. Phosphorylation of CPE binding factor by Eg2 regulates translation of c-mos mRNA. Nature, 2000, 404(6775): 302-307.
  • 4Palmer A, Gavin A C, Nebreda A R. A link between MAP kinase and p34(cdc2)/cyclin B during oocyte maturation:p90(rsk) phosphorylates and inactivates the p34(cdc2) inhibitory kinase Myt1. EMBO J, 1998, 17(17): 5037-5047.
  • 5Littlepage L E, Wu H, Andresson T, et al. Identification of phosphorylated residues that affect the activity of the mitotic kinase aurora-A. Proc Natl Acad Sci USA, 2002, 99(24):15440-15445.
  • 6Katayama H, Zhou H, Li Q, et al. Interaction and feedback regulation between STK15/BTAK/aurora-A kinase and protein phosphatase 1 through mitotic cell division cycle. J Biol Chem, 2001, 276(49): 46219-46224.
  • 7Chen S S, Chang P C, Cheng Y W, et al. Suppression of the STK15 oncogenic activity requires a transactivation-independent p53 function. EMBO J, 2002, 21(17): 4491-4499.
  • 8Kiat L S,Hui K M, Gopalan G. Aurora-A kinase interacting protein (AIP), a novel negative regulator of human aurora-A kinase. J Biol Chem. 2002, 277(47): 45558-45565.
  • 9Littlepage L E, Ruderman J V. Identification of a new APC/C recognition domain, the A box, which is required for the Cdh1-dependent destruction of the kinase aurora-A during mitotic exit. Genes Dev, 2002, 16(17): 2274-2285.
  • 10Bischoff J R, Plowman G D. The Aurora/Ip11p kinase family:regulators of chromosome segregation and cytokinesis.Trends Cell Biol, 1999, 9(11): 454-459.

共引文献13

同被引文献1

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部