ArticleCell cycle (Georgetown, Tex.)2014
DNA end resection is needed for the repair of complex lesions in G1-phase human cells.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 90 citations in OpenAlex.
- Activation of Pol theta-mediated end joining begins during mitotic commitment.bioRxiv : the preprint server for biology · 2026Article
- Base-excision repair increases DNA double-strand break clustering within heavy-ion tracks and modulates repair at δ-electron-induced breaks.Scientific reports · 2026Article
- Mechanisms and regulation of DNA end resection in the maintenance of genome stability.Nature reviews. Molecular cell biology · 2025Review
- Position in proton Bragg curve influences DNA damage complexity and survival in head and neck cancer cells.Clinical and translational radiation oncology · 2025Article
- 2-Deoxy-D-Glucose and ES-936 sensitize cancer- but not normal cells to both low- and high LET irradiation.Frontiers in oncology · 2025Article
- High-complexity of DNA double-strand breaks is key for alternative end-joining choice.Communications biology · 2024Article
- Potential Benefits of Combining Proton or Carbon Ion Therapy with DNA Damage Repair Inhibitors.Cells · 2024Review
- Characterization and regulation of cell cycle-independent noncanonical gene targeting.Nature communications · 2024Article
- A perspective on tumor radiation resistance following high-LET radiation treatment.Journal of cancer research and clinical oncology · 2024Review
- Key molecular DNA damage responses of human cells to radiation.Frontiers in cell and developmental biology · 2024Review
- High-LET charged particles: radiobiology and application for new approaches in radiotherapy.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023Review
- DNA damage and repair dependencies of ionising radiation modalities.Bioscience reports · 2023Review
- Simulating Space Conditions Evokes Different DNA Damage Responses in Immature and Mature Cells of the Human Hematopoietic System.International journal of molecular sciences · 2023Article
- Article
- DNA polymerase θ-mediated repair of high LET radiation-induced complex DNA double-strand breaks.Nucleic acids research · 2023Article
- The order of sequential exposure of U2OS cells to gamma and alpha radiation influences the formation and decay dynamics of NBS1 foci.PloS one · 2023Article
- Article
- Article
- DNA Damage Clustering after Ionizing Radiation and Consequences in the Processing of Chromatin Breaks.Molecules (Basel, Switzerland) · 2022Review
- Chromatin and the Cellular Response to Particle Radiation-Induced Oxidative and Clustered DNA Damage.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Repair of DNA double strand breaks (DSBs) is influenced by the chemical complexity of the lesion. Clustered lesions (complex DSBs) are generally considered more difficult to repair and responsible for early and late cellular effects after exposure to genotoxic agents. Resection is commonly used by the cells as part of the homologous recombination (HR) pathway in S- and G2-phase. In contrast, DNA resection in G1-phase may lead to an error-prone microhomology-mediated end joining. We induced DNA lesions with a wide range of complexity by irradiation of mammalian cells with X-rays or accelerated ions of different velocity and mass. We found replication protein A (RPA) foci indicating DSB resection both in S/G2- and G1-cells, and the fraction of resection-positive cells correlates with the severity of lesion complexity throughout the cell cycle. Besides RPA, Ataxia telangiectasia and Rad3-related (ATR) was recruited to complex DSBs both in S/G2- and G1-cells. Resection of complex DSBs is driven by meiotic recombination 11 homolog A (MRE11), CTBP-interacting protein (CtIP), and exonuclease 1 (EXO1) but seems not controlled by the Ku heterodimer or by phosphorylation of H2AX. Reduced resection capacity by CtIP depletion increased cell killing and the fraction of unrepaired DSBs after exposure to densely ionizing heavy ions, but not to X-rays. We conclude that in mammalian cells resection is essential for repair of complex DSBs in all phases of the cell-cycle and targeting this process sensitizes mammalian cells to cytotoxic agents inducing clustered breaks, such as in heavy-ion cancer therapy.
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