Journal
MOLECULAR CELL
Volume 47, Issue 4, Pages 497-510Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2012.07.029
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Funding
- Sir Henry Wellcome Fellowship
- Cancer Research UK
- ERC Advanced Investigator Grant (RecMitMei)
- Royal Society Wolfson Research Merit Award
- Cancer Research UK [11581] Funding Source: researchfish
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DNA double-strand breaks (DSBs) are highly toxic lesions that can drive genetic instability. To preserve gnome integrity, organisms have evolved several DSB repair mechanisms, of which nonhomologous end-joining (NHEJ) and homologous recombination (HR) represent the two most prominent. It has recently become apparent that multiple layers of regulation exist to ensure these repair pathways are accurate and restricted to the appropriate cellular contexts. Such regulation is crucial, as failure to properly execute DSB repair is known to accelerate tumorigenesis and is associated with several human genetic syndromes. Here, we review recent insights into the mechanisms that influence the choice between competing DSB repair pathways, how this is regulated during the cell cycle, and how imbalances in this equilibrium result in genome instability.
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