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细胞周期的演变

Evolution of the cell cycle.

作者信息

Nasmyth K

机构信息

Institute of Molecular Pathology, Vienna, Austria.

出版信息

Philos Trans R Soc Lond B Biol Sci. 1995 Sep 29;349(1329):271-81. doi: 10.1098/rstb.1995.0113.

DOI:10.1098/rstb.1995.0113
PMID:8577838
Abstract

Cell proliferation involves duplication of all cell constituents and their more-or-less equal segregation to daughter cells. It seems probable that the performance of primitive cell-like structures would have been dogged by poor duplication and segregation fidelity, and by parasitism. This favoured evolution of the genome and with it the distinction between 'genomic' components like chromosomes whose synthesis is periodic and most other 'functional' components whose synthesis is continuous. Eukaryotic cells evolved from bacterial ancestors whose fused genome was replicated from a single origin and whose means of segregating sister chromatids depended on fixing their identity at replication. Evolution of an endo- or cytoskeleton, initially as means of consuming other bacteria, eventually enabled evolution of the mitotic spindle and a new means of segregating sister chromatids whose replication could be initiated from multiple origins. In this primitive eukaryotic cell, S and M phases might have been triggered by activation of a single cyclin-dependent kinase whose destruction along with that of other proteins would have triggered anaphase. Mitotic non-disjunction would have greatly facilitated genomic expansion, now possible due to multiple origins, and thereby accelerated the tempo of evolution when permitted by environmental conditions.

摘要

细胞增殖涉及所有细胞成分的复制以及它们大致均等的向子细胞的分离。原始细胞样结构的表现可能一直受到复制和分离保真度差以及寄生现象的困扰。这有利于基因组的进化,随之而来的是像染色体这样合成是周期性的“基因组”成分与合成是连续的大多数其他“功能性”成分之间的区分。真核细胞从细菌祖先进化而来,其融合的基因组从单一原点复制,其分离姐妹染色单体的方式取决于在复制时确定它们的身份。内膜或细胞骨架的进化,最初是作为吞噬其他细菌的手段,最终促成了有丝分裂纺锤体的进化以及一种分离姐妹染色单体的新方式,其复制可以从多个原点启动。在这种原始真核细胞中,S期和M期可能由单一的细胞周期蛋白依赖性激酶的激活触发,该激酶与其他蛋白质一起被破坏会触发后期。有丝分裂不分离会极大地促进基因组扩展,由于有多个原点现在这成为可能,从而在环境条件允许时加速进化的节奏。

相似文献

1
Evolution of the cell cycle.细胞周期的演变
Philos Trans R Soc Lond B Biol Sci. 1995 Sep 29;349(1329):271-81. doi: 10.1098/rstb.1995.0113.
2
Model scenarios for evolution of the eukaryotic cell cycle.真核细胞周期演化的模型情景。
Philos Trans R Soc Lond B Biol Sci. 1998 Dec 29;353(1378):2063-76. doi: 10.1098/rstb.1998.0352.
3
The role of p53 in the response to mitotic spindle damage.p53在对有丝分裂纺锤体损伤反应中的作用。
Pathol Biol (Paris). 2000 Apr;48(3):246-54.
4
Multi-step control of spindle pole body duplication by cyclin-dependent kinase.细胞周期蛋白依赖性激酶对纺锤极体复制的多步骤控制
Nat Cell Biol. 2001 Jan;3(1):38-42. doi: 10.1038/35050543.
5
The mechanism of sister chromatid cohesion.姐妹染色单体黏连的机制。
Exp Cell Res. 2004 May 15;296(1):80-5. doi: 10.1016/j.yexcr.2004.03.005.
6
Building and breaking bridges between sister chromatids.构建和破坏姐妹染色单体之间的桥梁。
Bioessays. 2003 Dec;25(12):1178-91. doi: 10.1002/bies.10361.
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Segregating sister genomes: the molecular biology of chromosome separation.分离姐妹基因组:染色体分离的分子生物学
Science. 2002 Jul 26;297(5581):559-65. doi: 10.1126/science.1074757.
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Archaeal cell cycle progress.古菌细胞周期进程。
Curr Opin Microbiol. 2005 Dec;8(6):662-8. doi: 10.1016/j.mib.2005.10.008. Epub 2005 Oct 24.
9
Essential tension and constructive destruction: the spindle checkpoint and its regulatory links with mitotic exit.必要张力与建设性破坏:纺锤体检查点及其与有丝分裂退出的调控联系。
Biochem J. 2005 Feb 15;386(Pt 1):1-13. doi: 10.1042/BJ20041415.
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Regulation of cell cycle checkpoints by polo-like kinases.Polo样激酶对细胞周期检查点的调控。
Oncogene. 2005 Jan 10;24(2):277-86. doi: 10.1038/sj.onc.1208218.

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