ATM stabilizes DNA double-strand-break complexes during V(D)J recombination (original) (raw)
- Letter
- Published: 14 June 2006
- Girdhar G. Sharma2,
- Ching-Yu Huang1,
- Beth A. Helmink1,
- Laura M. Walker1,
- Katrina C. Khor1,
- Beth Nuskey3,
- Kathleen E. Sullivan4,
- Tej K. Pandita2,
- Craig H. Bassing3,5 &
- …
- Barry P. Sleckman1
Nature volume 442, pages 466–470 (2006)Cite this article
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Abstract
The ATM (ataxia-telangiectasia mutated) protein kinase mediates early cellular responses to DNA double-strand breaks (DSBs) generated during metabolic processes or by DNA-damaging agents1,2,3,4. ATM deficiency leads to ataxia-telangiectasia, a disease marked by lymphopenia, genomic instability and an increased predisposition to lymphoid malignancies with chromosomal translocations involving lymphocyte antigen receptor loci5,6. ATM activates cell-cycle checkpoints and can induce apoptosis in response to DNA DSBs1,2,3,4. However, defects in these pathways of the DNA damage response cannot fully account for the phenotypes of ATM deficiency. Here, we show that ATM also functions directly in the repair of chromosomal DNA DSBs by maintaining DNA ends in repair complexes generated during lymphocyte antigen receptor gene assembly. When coupled with the cell-cycle checkpoint and pro-apoptotic activities of ATM, these findings provide a molecular explanation for the increase in lymphoid tumours with translocations involving antigen receptor loci associated with ataxia-telangiectasia.
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Acknowledgements
We thank M. Schlissel for pMX-RSS-GFP/IRES-hCD4. STI571 was provided by Novartis Pharmaceuticals and KU-55933 was provided by G. Smith at KuDOS Pharmaceuticals. We thank H. Virgin, K. Murphy and M. Krangel for critical review of the manuscript. This work is supported in part by grants from the National Institutes of Health (to B.P.S. and T.K.P.) and the Department of Army (T.K.P.). C.H.B. is a Pew Scholar in the Biomedical Sciences and a recipient of a Pilot Project Award from the American Cancer Society. B.P.S. is a recipient of a Research Scholar Award from the American Cancer Society. C.-Y.H. is supported by a post-doctoral training grant and A.L.B. a pre-doctoral training grant from the NIH.
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Authors and Affiliations
- Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri, 63110, USA
Andrea L. Bredemeyer, Ching-Yu Huang, Beth A. Helmink, Laura M. Walker, Katrina C. Khor & Barry P. Sleckman - Department of Radiation Oncology, Washington University School of Medicine, St Louis, Missouri, 63110, USA
Girdhar G. Sharma & Tej K. Pandita - Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, 19104, USA
Beth Nuskey & Craig H. Bassing - Division of Allergy and Immunology, Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, 19104, USA
Kathleen E. Sullivan - Abramson Family Cancer Research Institute, Philadelphia, Pennsylvania, 19104, USA
Craig H. Bassing
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Correspondence toBarry P. Sleckman.
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Supplementary Notes
This file contains Supplementary Figures 1–19, Supplementary Methods and Supplementary Notes. The Supplementary Figures show the setup of the experimental system, data from additional cell lines, and controls for Figures 1-4. (PDF 2604 kb)
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Bredemeyer, A., Sharma, G., Huang, CY. et al. ATM stabilizes DNA double-strand-break complexes during V(D)J recombination.Nature 442, 466–470 (2006). https://doi.org/10.1038/nature04866
- Received: 05 January 2006
- Accepted: 03 May 2006
- Published: 14 June 2006
- Issue Date: 27 July 2006
- DOI: https://doi.org/10.1038/nature04866