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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Ataxia telangiectasia mutated (Atm) is not required for telomerase-mediated elongation of short telomeres
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Ataxia telangiectasia mutated (Atm) is not required for telomerase-mediated elongation of short telomeres

机译：端粒酶介导的短端粒伸长不需要共济失调毛细血管扩张突变（Atm）

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摘要

Telomerase-mediated telomere addition counteracts telomere shortening due to incomplete DNA replication. Short telomeres are the preferred substrate for telomere addition by telomerase; however, the mechanism by which telomerase recognizes short telomeres is unclear. In yeast, the Ataxia telangiectasia mutated (Atm) homolog, Tel1, is necessary for normal telomere length regulation likely by altering telomere structure, allowing telomerase recruitment to short telomeres. To examine the role of Atm in establishing preference for elongation of short telomeres in mice, we examined telomerase-mediated elongation of short dysfunctional telomeres in the presence or absence of Atm. Here we show that Atm is dispensable for elongation of short telomeres by telomerase, suggesting that telomerase recruitment in mammalian cells and in yeast may be regulated differently.
机译：由于DNA复制不完全，端粒酶介导的端粒添加可抵消端粒缩短。短端粒是通过端粒酶添加端粒的优选底物。然而，端粒酶识别短端粒的机制尚不清楚。在酵母中，共济失调的毛细血管扩张突变（Atm）同源物Tel1是正常端粒长度调节所必需的，可能通过改变端粒结构来实现，从而允许端粒酶募集至短端粒。若要检查Atm在建立小鼠短端粒延长偏好中的作用，我们检查了Atm存在或不存在时端粒酶介导的短功能障碍端粒延长。在这里，我们显示Atm是通过端粒酶延长短端粒所必需的，这表明在哺乳动物细胞和酵母菌中端粒酶募集可能受到不同的调节。

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