Format

Send to

Choose Destination
See comment in PubMed Commons below
Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2249-51. Epub 2006 Feb 7.

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

Author information

1
Department of Molecular Biology and Genetics and Graduate Program in Molecular Biology and Human Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21025, USA.

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.

PMID:
16467146
PMCID:
PMC1413760
DOI:
10.1073/pnas.0511143103
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Support Center