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端粒修剪在正常端粒长度动态变化中的作用。

The role of telomere trimming in normal telomere length dynamics.

机构信息

Children's Medical Research Institute and Sydney Medical School, University of Sydney, New South Wales, Australia.

出版信息

Cell Cycle. 2012 Apr 1;11(7):1309-15. doi: 10.4161/cc.19632.

DOI:10.4161/cc.19632
PMID:22421147
Abstract

Telomeres consist of repetitive DNA and associated proteins that protect chromosome ends from illicit DNA repair. It is well known that telomeric DNA is progressively eroded during cell division, until telomeres become too short and the cell stops dividing. There is a second mode of telomere shortening, however, which is a regulated form of telomere rapid deletion (TRD) termed telomere trimming that is reviewed here. Telomere trimming appears to involve resolution of recombination intermediate structures, which shortens the telomere by release of extrachromosomal telomeric DNA. This has been detected in human and in mouse cells and occurs both in somatic and germline cells, where it sets an upper limit on telomere length and contributes to a length equilibrium set-point in cells that have a telomere elongation mechanism. Telomere trimming thus represents an additional mechanism of telomere length control that contributes to normal telomere dynamics and cell proliferative potential.

摘要

端粒由重复 DNA 和相关蛋白组成,可保护染色体末端免受非法的 DNA 修复。众所周知,端粒 DNA 在细胞分裂过程中逐渐被侵蚀,直到端粒变得太短以至于细胞停止分裂。然而,端粒缩短还有第二种方式,这是一种受调控的端粒快速缺失(TRD)形式,称为端粒修剪,本文对此进行了综述。端粒修剪似乎涉及到重组中间体结构的解决,通过释放染色体外端粒 DNA 来缩短端粒。这在人和小鼠细胞中都有检测到,发生在体细胞和生殖细胞中,它为端粒长度设定了上限,并为具有端粒延长机制的细胞贡献了一个长度平衡设定点。因此,端粒修剪代表了一种额外的端粒长度控制机制,有助于正常的端粒动态和细胞增殖潜力。

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