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Science 26 February 1999:
Vol. 283. no. 5406, pp. 1321 - 1325
DOI: 10.1126/science.283.5406.1321
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Reports

p53- and ATM-Dependent Apoptosis Induced by Telomeres Lacking TRF2

Jan Karlseder, 1* Dominique Broccoli, 1*dagger Yumin Dai, 2 Stephen Hardy, 2ddagger Titia de Lange 1§

Although broken chromosomes can induce apoptosis, natural chromosome ends (telomeres) do not trigger this response. It is shown that this suppression of apoptosis involves the telomeric-repeat binding factor 2 (TRF2). Inhibition of TRF2 resulted in apoptosis in a subset of mammalian cell types. The response was mediated by p53 and the ATM (ataxia telangiectasia mutated) kinase, consistent with activation of a DNA damage checkpoint. Apoptosis was not due to rupture of dicentric chromosomes formed by end-to-end fusion, indicating that telomeres lacking TRF2 directly signal apoptosis, possibly because they resemble damaged DNA. Thus, in some cells, telomere shortening may signal cell death rather than senescence.

1 Laboratory for Cell Biology and Genetics, The Rockefeller University, New York, NY 10021, USA.
2 Cell Genesys, Foster City, CA 94405, USA.
*   These authors contributed equally to this work.

dagger    Present address: Fox Chase Cancer Center, 7701 Burholme Avenue, Philadelphia, PA 19111, USA.

ddagger    Present address: Chiron Corporation, 4560 Horton Street, Mailstop 4-3, Emeryville, CA 94608-2916, USA.

§   To whom correspondence should be addressed. E-mail: delange{at}rockvax.rockefeller.edu

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Topical DNA oligonucleotide therapy reduces UV-induced mutations and photocarcinogenesis in hairless mice.
D. A. Goukassian, E. Helms, H. van Steeg, C. van Oostrom, J. Bhawan, and B. A. Gilchrest (2004)
PNAS 101, 3933-3938
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Science. ISSN 0036-8075 (print), 1095-9203 (online)