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RESEARCH PAPER
1 Department of Genetics, 2 Department of Medicine, and 3 Department of Biochemistry and Molecular Pharmacology, Harvard Medical School and The Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA; 4 Department of Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
The BRCA1 gene product and its stoichiometric binding partner, BARD1, play a vital role in the cellular response to DNA damage. However, how they acquire specific biochemical functions after DNA damage is poorly understood. Following exposure to genotoxic stress, DNA damage-specific interactions were observed between BRCA1/BARD1 and the DNA damage-response proteins, TopBP1 and Mre11/Rad50/NBS1. Two distinct DNA damage-dependent super complexes emerged; their activation was dependent, in part, on the actions of specific checkpoint kinases, and each super complex contributed to a distinctive aspect of the DNA damage response. The results support a new, multifactorial model that describes how genotoxic stress enables BRCA1 to execute a diverse set of DNA damage-response functions.
[Keywords: BACH1; BARD1; BRCA1; CtIP; M/R/N; TopBP1]
Received October 3, 2005; revised version accepted November 2, 2005.
Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.1381306.
5 These authors contributed equally to this work.
E-MAIL david_livingston{at}dfci.harvard.edu; FAX (617) 632-4381.
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