53BP1 promotes non-homologous end joining of telomeres by increasing chromatin mobility

Nadya Dimitrova, Yi-Chun M. Chen, David L. Spector and Titia de Lange ()
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Nadya Dimitrova: The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA
Yi-Chun M. Chen: Cold Spring Harbor Laboratory, One Bungtown Road, Cold Spring Harbor, New York 11724, USA
David L. Spector: Cold Spring Harbor Laboratory, One Bungtown Road, Cold Spring Harbor, New York 11724, USA
Titia de Lange: The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA

Nature, 2008, vol. 456, issue 7221, 524-528

Abstract: DNA repair: 53BP1 puts ends in motion When either exogenous or endogenous double-strand breaks occur, the p53 binding protein 53BP1 is one of the earliest proteins to be recruited to the site of the break. 53BP1 helps to promote rejoining of DNA ends during class switch recombination; in a pair of papers in this week's Nature, the laboratories of André Nussenzweig and Titia de Lange show it is also required for V(D)J recombination and for joining of DNA breaks in telomeres. In V(D)J recombination, the ends of the programmed double-strand break are degraded when 53BP1 is absent, and joining between distal V and DJ segments is affected. At broken telomeres, 53BP1 increases the volume of the nucleus searched by the DNA ends so that they are more likely to encounter a partner to which they can be ligated. Thus, 53BP1 facilitates repair by changing the dynamics of movement of broken ends, making long-range interactions more frequent.

Date: 2008
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DOI: 10.1038/nature07433

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