Ataxia telangiectasia mutated (Atm) is not required for telomerase-mediated elongation of short telomeres

David Feldser, Margaret A. Strong, Carol W. Greider

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)2249-2251
Number of pages3
JournalProceedings of the National Academy of Sciences of the United States of America
Volume103
Issue number7
DOIs
StatePublished - Feb 14 2006

Keywords

  • Chromosome fusion
  • DNA damage
  • Telomerase recruitment

ASJC Scopus subject areas

  • General

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