ArticlePLoS genetics2016
53BP1 Protects against CtIP-Dependent Capture of Ectopic Chromosomal Sequences at the Junction of Distant Double-Strand Breaks.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- PKA prevents the resection of DNA double-strand breaks and favours nonhomologous end-joining.Scientific reports · 2025Article
- Genome rearrangements induced by the stimulation of end-joining of DNA double strand breaks through multiple phosphorylation of MRE11 by the kinase PKB/AKT1.Nucleic acids research · 2025Article
- BRD2 promotes antibody class switch recombination by facilitating DNA repair in collaboration with NIPBL.Nucleic acids research · 2024Article
- A novel RBBP8(p.E281*) germline mutation is a predisposing mutation in familial hereditary cancer syndrome.Journal of molecular medicine (Berlin, Germany) · 2023Article
- To indel or not to indel: Factors influencing mutagenesis during chromosomal break end joining.DNA repair · 2022Review
- RAD51 protects against nonconservative DNA double-strand break repair through a nonenzymatic function.Nucleic acids research · 2022Article
- Phospho-Ku70 induced by DNA damage interacts with RNA Pol II and promotes the formation of phospho-53BP1 foci to ensure optimal cNHEJ.Nucleic acids research · 2021Article
- An Efficient Clustered Regularly Interspaced Short Palindromic Repeat (CRISPR)/CRISPR-Associated Protein 9 Mutagenesis System for Oil Palm (Frontiers in plant science · 2021Article
- The molecular basis and disease relevance of non-homologous DNA end joining.Nature reviews. Molecular cell biology · 2020Review
- DNA Damage: From Threat to Treatment.Cells · 2020Review
- RNF8 has both KU-dependent and independent roles in chromosomal break repair.Nucleic acids research · 2020Article
- DNA double-strand break repair-pathway choice in somatic mammalian cells.Nature reviews. Molecular cell biology · 2019Review
- Microhomologies are prevalent at Cas9-induced larger deletions.Nucleic acids research · 2019Article
- Pharmacological boost of DNA damage response and repair by enhanced biogenesis of DNA damage response RNAs.Scientific reports · 2019Article
- Regulation of DNA Double Strand Breaks Processing: Focus on Barriers.Frontiers in molecular biosciences · 2019Review
- Transition from a meiotic to a somatic-like DNA damage response during the pachytene stage in mouse meiosis.PLoS genetics · 2019Article
- Harnessing accurate non-homologous end joining for efficient precise deletion in CRISPR/Cas9-mediated genome editing.Genome biology · 2018Article
- High doses of CRISPR/Cas9 ribonucleoprotein efficiently induce gene knockout with low mosaicism in the hydrozoan Clytia hemisphaerica through microhomology-mediated deletion.Scientific reports · 2018Article
- Repair of a Site-Specific DNA Cleavage: Old-School Lessons for Cas9-Mediated Gene Editing.ACS chemical biology · 2018Review
- PARP2 controls double-strand break repair pathway choice by limiting 53BP1 accumulation at DNA damage sites and promoting end-resection.Nucleic acids research · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
DNA double-strand breaks (DSB) are very harmful lesions that can generate genome rearrangements. In this study, we used intrachromosomal reporters to compare both the efficiency and accuracy of end-joining occurring with close (34 bp apart) vs. distant DSBs (3200 bp apart) in human fibroblasts. We showed that a few kb between two intrachromosomal I-SceI-induced DSBs are sufficient to foster deletions and capture/insertions at the junction scar. Captured sequences are mostly coupled to deletions and can be partial duplications of the reporter (i.e., sequences adjacent to the DSB) or insertions of ectopic chromosomal sequences (ECS). Interestingly, silencing 53BP1 stimulates capture/insertions with distant but not with close double-strand ends (DSEs), although deletions were stimulated in both case. This shows that 53BP1 protects both close and distant DSEs from degradation and that the association of unprotection with distance between DSEs favors ECS capture. Reciprocally, silencing CtIP lessens ECS capture both in control and 53BP1-depleted cells. We propose that close ends are immediately/rapidly tethered and ligated, whereas distant ends first require synapsis of the distant DSEs prior to ligation. This "spatio-temporal" gap gives time and space for CtIP to initiate DNA resection, suggesting an involvement of single-stranded DNA tails for ECS capture. We therefore speculate that the resulting single-stranded DNA copies ECS through microhomology-mediated template switching.
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