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Mol Cell. 2012 Aug 24;47(4):497-510. doi: 10.1016/j.molcel.2012.07.029.

Playing the end game: DNA double-strand break repair pathway choice.

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1
London Research Institute, Clare Hall Laboratories, Blanche Lane, South Mimms EN6 3LD, UK.

Abstract

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.

PMID:
22920291
DOI:
10.1016/j.molcel.2012.07.029
[Indexed for MEDLINE]
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