端粒酶逆转录酶（ALT）通过借鉴减数分裂来实现移动。
ALT telomeres borrow from meiosis to get moving.
作者信息
Arnoult Nausica, Karlseder Jan
机构信息
The Salk Institute for Biological Studies, Molecular and Cell Biology Laboratory, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.
The Salk Institute for Biological Studies, Molecular and Cell Biology Laboratory, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.
出版信息
Cell. 2014 Sep 25;159(1):11-12. doi: 10.1016/j.cell.2014.09.013.
Abstract
Telomere clustering is required for the homologous recombination events that maintain chromosome ends in cells relying on alternative lengthening of telomeres (ALT). New data demonstrate that damage signaling at telomeres, a likely step in activating maintenance mechanisms, induces directional movement and synapsis driven by the machinery responsible for recombination in meiosis.
摘要
端粒聚集是依赖端粒替代延长（ALT）来维持染色体末端的细胞中同源重组事件所必需的。新数据表明，端粒处的损伤信号传导（这可能是激活维持机制的一个步骤）会诱导由减数分裂中负责重组的机制驱动的定向移动和联会。
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