ArticleNucleic acids research2013
Competing roles of DNA end resection and non-homologous end joining functions in the repair of replication-born double-strand breaks by sister-chromatid recombination.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Asymmetrical recognition and processing of double-strand breaks formed during DNA replication.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The optimal strategy balancing risk and speed predicts DNA damage checkpoint override times.Nature physics · 2022Article
- Rpd3L and Hda1 histone deacetylases facilitate repair of broken forks by promoting sister chromatid cohesion.Nature communications · 2019Article
- Guidelines for DNA recombination and repair studies: Cellular assays of DNA repair pathways.Microbial cell (Graz, Austria) · 2019Review
- A genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection.Nature communications · 2016Article
- Assays for DNA double-strand break repair by microhomology-based end-joining repair mechanisms.Nucleic acids research · 2016Article
- Recombinational repair of radiation-induced double-strand breaks occurs in the absence of extensive resection.Nucleic acids research · 2016Article
- EXO1 is critical for embryogenesis and the DNA damage response in mice with a hypomorphic Nbs1 allele.Nucleic acids research · 2015Article
- RNA polymerase II contributes to preventing transcription-mediated replication fork stalls.The EMBO journal · 2015Article
- RAD51 potentiates synergistic effects of chemotherapy with PCI-24781 and cis-diamminedichloroplatinum on gastric cancer.World journal of gastroenterology · 2014Article
- Roles of exonucleases and translesion synthesis DNA polymerases during mitotic gap repair in yeast.DNA repair · 2013Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
While regulating the choice between homologous recombination and non-homologous end joining (NHEJ) as mechanisms of double-strand break (DSB) repair is exerted at several steps, the key step is DNA end resection, which in Saccharomyces cerevisiae is controlled by the MRX complex and the Sgs1 DNA helicase or the Sae2 and Exo1 nucleases. To assay the role of DNA resection in sister-chromatid recombination (SCR) as the major repair mechanism of spontaneous DSBs, we used a circular minichromosome system for the repair of replication-born DSBs by SCR in yeast. We provide evidence that MRX, particularly its Mre11 nuclease activity, and Sae2 are required for SCR-mediated repair of DSBs. The phenotype of nuclease-deficient MRX mutants is suppressed by ablation of Yku70 or overexpression of Exo1, suggesting a competition between NHEJ and resection factors for DNA ends arising during replication. In addition, we observe partially redundant roles for Sgs1 and Exo1 in SCR, with a more prominent role for Sgs1. Using human U2OS cells, we also show that the competitive nature of these reactions is likely evolutionarily conserved. These results further our understanding of the role of DNA resection in repair of replication-born DSBs revealing unanticipated differences between these events and repair of enzymatically induced DSBs.
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