Journal
MOLECULAR CELL
Volume 33, Issue 3, Pages 335-343Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2009.01.016
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Funding
- Max Planck Society
- Center for Integrated Protein Science Munich
- German Cancer Foundation
- RUBICON EU Network of Excellence
- Boehringer Ingelheim Ph.D. scholarships
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DNA double-strand breaks (DSBs) are acutely hazardous for cells, as they can cause genome instability. DSB repair involves the sequential recruitment of repair factors to the DSBs, followed by Rad51 mediated homology probing, DNA synthesis, and ligation. However, little is known about how cells react if no homology is found and DSBs persist. Here, by monitoring a single persistent DNA break, we show that, following DNA resection and RPA recruitment, Rad51 spreads chromosome-wide bidirectionally from the DSB but selectively only on the broken chromosome. Remarkably, the persistent DSB is later fixed to the nuclear periphery in a process that requires Rad51, the histone variant H2A.Z, its SUMO modification, and the DNA-damage checkpoint. Indeed, H2A.Z is deposited close to the break early but transiently and directs DNA resection, single DSB-induced checkpoint activation, and DSB anchoring. Thus, a persistent DSB induces a multifaceted response, which is linked to a specific chromatin mark.
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