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Annu Rev Genet. 2011;45:247-71. doi: 10.1146/annurev-genet-110410-132435. Epub 2011 Sep 12.

Double-strand break end resection and repair pathway choice.

Author information

1
Department of Microbiology & Immunology, Columbia University Medical Center, New York, New York 10032, USA. lss5@columbia.edu

Abstract

DNA double-strand breaks (DSBs) are cytotoxic lesions that can result in mutagenic events or cell death if left unrepaired or repaired inappropriately. Cells use two major pathways for DSB repair: nonhomologous end joining (NHEJ) and homologous recombination (HR). The choice between these pathways depends on the phase of the cell cycle and the nature of the DSB ends. A critical determinant of repair pathway choice is the initiation of 5'-3' resection of DNA ends, which commits cells to homology-dependent repair, and prevents repair by classical NHEJ. Here, we review the components of the end resection machinery, the role of end structure, and the cell-cycle phase on resection and the interplay of end processing with NHEJ.

[Indexed for MEDLINE]

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