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Nucleic Acids Research Advance Access originally published online on February 7, 2008
Nucleic Acids Research 2008 36(5):1741-1754; doi:10.1093/nar/gkn026
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Nucleic Acids Research, 2008, Vol. 36, No. 5 1741-1754
© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

Role of ATM in the telomere response to the G-quadruplex ligand 360A

Gaëlle Pennarun1, Christine Granotier1, Françoise Hoffschir1, Eliane Mandine2, Denis Biard3, Laurent R. Gauthier1 and François D. Boussin1,*

1CEA, DSV, iRCM, Laboratoire de Radiopathologie-IPSC, 92265 Fontenay-aux-Roses, 2Aventis Pharma SA, Centre de Recherche de Paris, 94403 Vitry-sur-Seine and 3CEA, DSV, iRCM, Laboratoire de Génétique de la Radiosensibilité, 92265 Fontenay-aux-Roses, France

*To whom correspondence should be addressed. Tel: +33 1 46 54 97 91; Fax: +33 1 46 54 97 02; Email: boussin{at}cea.fr

Received October 29, 2007. Revised January 16, 2008. Accepted January 16, 2008.

Telomeres are known to prevent chromosome ends from being recognized as DNA double-strand breaks. Conversely, many DNA damage response proteins, including ATM, are thought to participate to telomere maintenance. However, the precise roles of ATM at telomeres remain unclear due to its multiple functions in cell checkpoints and apoptosis. To gain more insights into the role of ATM in telomere maintenance, we determined the effects of the G-quadruplex ligand 360A in various cell lines lacking functional ATM. We showed, by using Fluorescence in situ hybridization (FISH) and Chromosome Orientation-FISH using telomere PNA probes, that 360A induced specific telomere aberrations occurring during or after replication, mainly consisting in sister telomere fusions and also recombinations that involved preferentially the lagging strand telomeres. We demonstrate that ATM reduced telomere instability independently of apoptosis induction. Our results suggest thus that ATM has a direct role in preventing inappropriate DNA repair at telomeres, which could be related to its possible participation to the formation of protected structures at telomeres.

The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors.


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