ArticleNucleic acids research2016
The structure of ends determines the pathway choice and Mre11 nuclease dependency of DNA double-strand break repair.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Integrative Computational Analysis of Common EXO5 Haplotypes: Impact on Protein Dynamics, Genome Stability, and Cancer Progression.Journal of chemical information and modeling · 2025Article
- Review
- The repair of topoisomerase 2 cleavage complexes in Arabidopsis.The Plant cell · 2022Article
- DNA damage repair: historical perspectives, mechanistic pathways and clinical translation for targeted cancer therapy.Signal transduction and targeted therapy · 2021Review
- CST in maintaining genome stability: Beyond telomeres.DNA repair · 2021Review
- Polθ promotes the repair of 5'-DNA-protein crosslinks by microhomology-mediated end-joining.Cell reports · 2021Article
- MRE11-RAD50-NBS1 Complex Is Sufficient to Promote Transcription by RNA Polymerase II at Double-Strand Breaks by Melting DNA Ends.Cell reports · 2021Article
- DNA Double Strand Break Repair Pathways in Response to Different Types of Ionizing Radiation.Frontiers in genetics · 2021Review
- Off-Target Analysis in Gene Editing and Applications for Clinical Translation of CRISPR/Cas9 in HIV-1 Therapy.Frontiers in genome editing · 2021Review
- Metastasis Suppressor NME1 Modulates Choice of Double-Strand Break Repair Pathways in Melanoma Cells by Enhancing Alternative NHEJ while Inhibiting NHEJ and HR.International journal of molecular sciences · 2020Article
- CtIP promotes the motor activity of DNA2 to accelerate long-range DNA end resection.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Adjacent mutations in the archaeal Rad50 ABC ATPase D-loop disrupt allosteric regulation of ATP hydrolysis through different mechanisms.Nucleic acids research · 2020Article
- CNCC: an analysis tool to determine genome-wide DNA break end structure at single-nucleotide resolution.BMC genomics · 2020Article
- MRE11-RAD50-NBS1 complex alterations and DNA damage response: implications for cancer treatment.Molecular cancer · 2019Review
- Purification and Biophysical Characterization of the Mre11-Rad50-Nbs1 Complex.Methods in molecular biology (Clifton, N.J.) · 2019Article
- The MRE11-RAD50-NBS1 Complex Conducts the Orchestration of Damage Signaling and Outcomes to Stress in DNA Replication and Repair.Annual review of biochemistry · 2018Review
- Dna2 initiates resection at clean DNA double-strand breaks.Nucleic acids research · 2017Article
- CtIP/Ctp1/Sae2, molecular form fit for function.DNA repair · 2017Review
- Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The key event in the choice of repair pathways for DNA double-strand breaks (DSBs) is the initial processing of ends. Non-homologous end joining (NHEJ) involves limited processing, but homology-dependent repair (HDR) requires extensive resection of the 5' strand. How cells decide if an end is channeled to resection or NHEJ is not well understood. We hypothesize that the structure of ends is a major determinant and tested this hypothesis with model DNA substrates in Xenopus egg extracts. While ends with normal nucleotides are efficiently channeled to NHEJ, ends with damaged nucleotides or bulky adducts are channeled to resection. Resection is dependent on Mre11, but its nuclease activity is critical only for ends with 5' bulky adducts. CtIP is absolutely required for activating the nuclease-dependent mechanism of Mre11 but not the nuclease-independent mechanism. Together, these findings suggest that the structure of ends is a major determinant for the pathway choice of DSB repair and the Mre11 nuclease dependency of resection.
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