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Molecular and Cellular Biology, September 2008, p. 5724-5735, Vol. 28, No. 18
0270-7306/08/$08.00+0     doi:10.1128/MCB.01764-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

No Overt Nucleosome Eviction at Deprotected Telomeres {triangledown} ,{dagger}

Peng Wu and Titia de Lange*

Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, New York 10021

Received 26 September 2007/ Returned for modification 31 October 2007/ Accepted 2 July 2008

Dysfunctional telomeres elicit the canonical DNA damage response, which includes the activation of the ATM or ATR kinase signaling pathways and end processing by nonhomologous end joining (NHEJ) or homologous recombination (HR). The cellular response to DNA double-strand breaks has been proposed to involve chromatin remodeling and nucleosome eviction, but whether dysfunctional telomeres undergo chromatin reorganization is not known. Here, we report on the nucleosomal organization of telomeres that have become deprotected through the deletion of the shelterin components TRF2 or POT1. We found no evidence of changes in the nucleosomal organization of the telomeric chromatin or nucleosome eviction near the telomere terminus. An unaltered chromatin structure was observed at telomeres lacking TRF2, which activate the ATM kinase and are a substrate for NHEJ. Similarly, telomeres lacking POT1a and POT1b, which activate the ATR kinase, showed no overt nucleosome eviction. Finally, telomeres lacking TRF2 and Ku70, which are processed by HR, appeared to maintain their original nucleosomal organization. We conclude that ATM signaling, ATR signaling, NHEJ, and HR at deprotected telomeres can take place in the absence of overt nucleosome eviction.

* Corresponding author. Mailing address: The Rockefeller University, 1230 York Avenue, New York, NY 10021. Phone: (212) 327-8146. Fax: (212) 327-7147. E-mail: delange{at}mail.rockefeller.edu

{triangledown} Published ahead of print on 14 July 2008.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, September 2008, p. 5724-5735, Vol. 28, No. 18
0270-7306/08/$08.00+0     doi:10.1128/MCB.01764-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Oganesian, L., Karlseder, J. (2009). Telomeric armor: the layers of end protection. J. Cell Sci. 122: 4013-4025 [Abstract] [Full Text]  
  • Zeitlin, S. G., Baker, N. M., Chapados, B. R., Soutoglou, E., Wang, J. Y. J., Berns, M. W., Cleveland, D. W. (2009). Double-strand DNA breaks recruit the centromeric histone CENP-A. Proc. Natl. Acad. Sci. USA 106: 15762-15767 [Abstract] [Full Text]  
  • Baker, A. M., Fu, Q., Hayward, W., Lindsay, S. M., Fletcher, T. M. (2009). The Myb/SANT domain of the telomere-binding protein TRF2 alters chromatin structure. Nucleic Acids Res 37: 5019-5031 [Abstract] [Full Text]  


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