Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 103, Issue 7, Pages 2249-2251Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0511143103
Keywords
DNA damage; chromosome fusion; telomerase recruitment
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Funding
- NCI NIH HHS [P01 CA016519, P01 CA16519] Funding Source: Medline
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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.
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