Telomerase misbehaves after a breakup Suppressing telomerase action at broken DNA preserves genome integrity
成果类型：
Editorial Material
署名作者：
Arnoult, Nausica; Cech, Thomas R.
署名单位：
University of Colorado System; University of Colorado Boulder; University of Colorado System; University of Colorado Boulder; University of Colorado System; University of Colorado Boulder
刊物名称：
SCIENCE
ISSN/ISSBN：
0036-9210
DOI：
10.1126/science.adn7791
发表日期：
2024-02-16
页码：
702-703
关键词：
摘要：
Cells must distinguish between broken chromosome ends and natural ends, or telomeres. Broken chromosomes require repair, but telomeres need to be protected from repair because joining two telomeres would result in disastrous chromosome fusions. Telomerase is the enzyme that maintains chromosome ends by adding repeated DNA sequences. If directed to a DNA break, telomerase would erroneously create a new telomere, precipitating the loss of essential genetic material distal from the break site. Although extensive research has elucidated how telomeres evade DNA repair pathways, the question of telomerase's misguided activity at DNA breaks in human cells has remained enigmatic. On page 763 of this issue, Kinzig et al. (1) report that telomerase can cause harmful neotelomere formation in human cells. They also show that such events are kept to a minimum by the naturally low prevalence of telomerase and the intervention of the ataxia telangiectasia and Rad3-related (ATR) cellular signaling pathway.