ArticleNucleic acids research2007
Capture of linear fragments at a double-strand break in yeast.
Article in Nucleic acids research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Non-canonical gene amplifications facilitate adaptive evolution in bacteria.Nature microbiology · 2026Article
- A more significant role for insertion sequences in large-scale rearrangements in bacterial genomes.mBio · 2025Article
- Non-homologous DNA increases gene disruption efficiency by altering DNA repair outcomes.Nature communications · 2016Article
- Article
- End-processing during non-homologous end-joining: a role for exonuclease 1.Nucleic acids research · 2011Article
- Intron creation and DNA repair.Cellular and molecular life sciences : CMLS · 2011Review
- Zinc-finger nuclease-driven targeted integration into mammalian genomes using donors with limited chromosomal homology.Nucleic acids research · 2010Article
- Chromosomal translocations caused by either pol32-dependent or pol32-independent triparental break-induced replication.Molecular and cellular biology · 2009Article
- Mechanisms of change in gene copy number.Nature reviews. Genetics · 2009Review
- Human Rad52-mediated homology search and annealing occurs by continuous interactions between overlapping nucleoprotein complexes.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- RAD59 is required for efficient repair of simultaneous double-strand breaks resulting in translocations in Saccharomyces cerevisiae.DNA repair · 2008Article
- Proofreading activity of DNA polymerase Pol2 mediates 3'-end processing during nonhomologous end joining in yeast.PLoS genetics · 2008Article
- Genetic Susceptibility to Rhodococcus equi.Journal of veterinary internal medicineReview
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Double-strand breaks (DSBs) are dangerous chromosomal lesions that must be efficiently repaired in order to avoid loss of genetic information or cell death. In all organisms studied to date, two different mechanisms are used to repair DSBs: homologous recombination (HR) and non-homologous end joining (NHEJ). Previous studies have shown that during DSB repair, non-homologous exogenous DNA (also termed 'filler DNA') can be incorporated at the site of a DSB. We have created a genetic system in the yeast Saccharomyces cerevisiae to study the mechanism of fragment capture. Our yeast strains carry recognition sites for the HO endonuclease at a unique chromosomal site, and plasmids in which a LEU2 gene is flanked by HO cut sites. Upon induction of the HO endonuclease, a linear extrachromosomal fragment is generated in each cell and its incorporation at the chromosomal DSB site can be genetically monitored. Our results show that linear fragments are captured at the repaired DSB site at frequencies of 10(-6) to 10(-4) per plated cell depending on strain background and specific end sequences. The mechanism of fragment capture depends on the NHEJ machinery, but only partially on the homologous recombination proteins. More than one fragment can be used during repair, by a mechanism that relies on the annealing of small complementary sequences. We present a model to explain the basis for fragment capture.
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