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DNA double-strand breaks (DSBs) are highly toxic lesions that can drive genetic instability. To preserve genome 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.

Original publication

DOI

10.1016/j.molcel.2012.07.029

Type

Journal article

Journal

Mol Cell

Publication Date

24/08/2012

Volume

47

Pages

497 - 510

Keywords

Animals, Cell Cycle, DNA Breaks, Double-Stranded, DNA Repair, Genomic Instability, Humans, Recombination, Genetic