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.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Animals
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Cell Cycle
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DNA Breaks, Double-Stranded*
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DNA End-Joining Repair*
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DNA Helicases / chemistry
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DNA Helicases / genetics
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Exodeoxyribonucleases / chemistry
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Exodeoxyribonucleases / genetics
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Fanconi Anemia / genetics
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Gene Expression Regulation, Fungal
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Genes, BRCA1
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Genes, Fungal*
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Genes, cdc
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Humans
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Protein Conformation
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Recombinational DNA Repair
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Saccharomyces cerevisiae / chemistry
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Saccharomyces cerevisiae / genetics*
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Saccharomyces cerevisiae Proteins / chemistry
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Saccharomyces cerevisiae Proteins / genetics
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Translocation, Genetic
Substances
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Saccharomyces cerevisiae Proteins
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Exodeoxyribonucleases
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exodeoxyribonuclease I
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DNA Helicases
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DNA2 protein, S cerevisiae