Abstract

The integrity of the genome is frequently challenged by double-strand breaks in the DNA. Defects in the cellular response to double-strand breaks are a major cause of cancer and other age-related pathologies; therefore, much effort has been directed at understanding the enzymatic mechanisms involved in recognizing, signalling and repairing double-strand breaks. Recent work indicates that chromatin — the fibres into which DNA is packaged with a proteinaceous structural polymer — has an important role in initiating, propagating and terminating this cellular response to DNA damage.

1. MRC Genome Damage and Stability Centre, University of Sussex, Brighton BN1 9RQ, UK.
2. Howard Hughes Medical Institute, The Rockefeller University, 1230 York Avenue, New York, New York 10021, USA.
3. Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, 10 Center Drive, 4B04, Bethesda, Maryland 20892, USA.

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