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Mechanisms and Consequences of Double‐Strand DNA Break Formation in Chromatin
Open accessAbstract
All organisms suffer double‐strand breaks (DSBs) in their DNA as a result of exposure to ionizing radiation. DSBs can also form when replication forks encounter DNA lesions or repair intermediates. The processing and repair of DSBs can lead to mutations, loss of heterozygosity, and chromosome rearrangements that result in cell death or cancer. The most common pathway used to repair DSBs in metazoans (non‐homologous DNA end joining) is more commonly mutagenic than the alternative pathway (homologous recombination mediated repair). Thus, factors that influence the choice of pathways used DSB repair can affect an individual's mutation burden and risk of cancer. This review describes radiological, chemical, and biological mechanisms that generate DSBs, and discusses the impact of such variables as DSB etiology, cell type, cell cycle, and chromatin structure on the yield, distribution, and processing of DSBs. The final section focuses on nucleosome‐specific mechanisms that influence DSB production, and the possible relationship between higher order chromosome coiling and chromosome shattering (chromothripsis). J. Cell. Physiol. 230: 3–14, 2016. © 2015 Wiley Periodicals, Inc.
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“SSBs may form DSBs through their collision with the transcriptional machinery and replication forks, or through their close proximity to another SSB.”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Cannan & Pederson, 2016
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“DSBs are also directly generated by transcription (Cannan & Pederson, 2016), whereby topoisomerase II (TOP2) induces transient DSBs to relieve torsional stress and facilitate gene expression.”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Cannan & Pederson, 2016
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“DNA double-strand breaks (DSB) induced by radiation, toxic chemicals or endogenous processes are the most serious DNA damage resulting in genome instability and cell death (Cannan & Pederson, 2016).”
BackgroundTowards the genomic sequence code of DNA fragility for machine learning
Pflughaupt, P., Abdullah, A. A., Masuda, K., & Sahakyan, A. B. (2024) · Nucleic Acids Research · doi:10.1093/nar/gkae914 · Cited by 4
Cell-cycle dependent DNA repair and replication unifies patterns of chromosome instability
Lu, B., Winnall, S., Cross, W. C. H., & Barnes, C. P. (2025) · Nature Communications · doi:10.1038/s41467-025-58245-z · Cited by 5
“Although NHEJ occurs throughout the cell cycle, it mainly occurs in G 1 due to the absence of homologous sequences, such as sister chromatids, which are required for HR 66 .”
Wang, Y., Hess, J. D., Wang, C., Ma, L., Luo, M., Jossart, J. N., Perry, J. J., Kwon, D., Wang, Z., Pei, X., et al. (2025) · ACS Chemical Biology · doi:10.1021/acschembio.5c00117 · Cited by 5
“Finally, we evaluated the stability of purified EXO1 protein in a reaction buffer maintained on ice for 1, 2, 4, 8, 12, or 16 h.”
Distinct functions of PAXX and MRI during chromosomal end joining
Cisneros‐Aguirre, M., Lopezcolorado, F. W., Ping, X., Chen, R., & Stark, J. M. (2025) · iScience · doi:10.1016/j.isci.2025.112722 · Cited by 6
A reporter mouse for in vivo detection of DNA damage in embryonic germ cells
Bloom, J. C., & Schimenti, J. C. (2020) · genesis · doi:10.1002/dvg.23368 · Cited by 5
Chromosome Banding and Mechanism of Chromosome Aberrations
Kumar, S., Kiso, A., & Kithan, N. A. (2021) · IntechOpen eBooks · doi:10.5772/intechopen.96242 · Cited by 5
Poly adenosine diphosphate-ribosylation, a promising target for colorectal cancer treatment
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Double-strand breaks quantification by statistical length analysis of DNA fragments imaged with AFM
Sofińska, K., Cieśla, M., Barbasz, J., Wilkosz, N., Lipiec, E. W., Szymoński, M., & Białas, P. (2022) · Measurement · doi:10.1016/j.measurement.2022.111362 · Cited by 5
Roberts, A. H., Bowen, J. E., Zhou, X., Burke, I., Wenaas, M. H., Blake, T. A., Timmons, S. C., & Kuzmanov, A. (2022) · Toxicology and Industrial Health · doi:10.1177/07482337221117357 · Cited by 5
“Recombination defects prevent the proper alignment and segregation of chromosomes in the first meiotic division (Cannan and Pederson, 2016; Gray and Cohen, 2016; Murakami and Keeney, 2008).”
BackgroundAutomated modeling of protein accumulation at DNA damage sites using qFADD.py
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SMC protein RecN drives RecA filament translocation and remodelling for in vivo homology searchPreprint
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The eye lens as an aging paradigm par excellence
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A non-tethering role for the Drosophila Pol θ linker domain in promoting damage resolution
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“DNA double-strand breaks (DSBs) are harmful DNA lesions that can be induced by exogenous agents, such as ionizing radiation (IR), or normal cellular processes, such as DNA replication and transcription [ 1 ].”
Alshareedah, I., Pangeni, S., Dewan, P. A., Honda, M., Liao, T.-W., Spies, M., & Ha, T. (2026) · Nucleic Acids Research · doi:10.1093/nar/gkag043 · Cited by 4
“Among the forms of DNA damage, double-strand breaks (DSBs) are the most lethal and can occur during DNA metabolism or result from reactive oxygen species and irradiation [ 4 ].”
How to Shift the Equilibrium of DNA Break Repair in Favor of Homologous Recombination
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Senataxin Attenuates DNA Damage Response Activation and Suppresses Senescence
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“DSBs also occur by exposure to exogenous DNA damaging agents, including ionizing radiation and radiomimetic chemicals [7].”
GDBr: genomic signature interpretation tool for DNA double-strand break repair mechanisms
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MRE11-RAD50-NBS1-CtIP: one key nuclease ensemble functions in the maintenance of genome stability
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Effect of curcumin on γ–ray-induced cell response
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“They could result in either loss or rearrangement of genetic information, cell death or malignant transformation [7].”
BackgroundEl‐Kamand, S., Adams, M. N., Matthews, J. M., Plessis, M. D., Crossett, B., Connolly, A. M., Breen, N., Dudley, A., Richard, D. J., Gamsjaeger, R., et al. (2023) · Protein Science · doi:10.1002/pro.4782 · Cited by 4
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Synthesis and Evaluation of (Bis)benzyltetrahydroisoquinoline Alkaloids as Antiparasitic Agents
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Stitching up broken DNA ends by FANCA
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“Still, it is possible that FANCA and RAD52 are mediating SSA repair through slightly differing mechanisms, due to the variety and complexity of DSB substrates that can arise as a result of different damage sources.(9) SSA repair through either FANCA or RAD52 may also be tissue-specific, as FANCA shows increased levels…”
BackgroundNebenfuehr, B., Sanford, L., Taylor, E. R., Ball, K. A., Woods-Killam, C. E., Ghasemi, H. I., Proctor, B., Ortega, R., Sempeck, C., Dowell, R. D., et al. (2026) · Cell Reports · doi:10.1016/j.celrep.2025.116850 · Cited by 4
Chromosomal breaks at the origin of small tandem DNA duplications
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“or (ii) indirectly, by converting water molecules into reactive oxygen species (ROS) that subsequently can react with DNA to from SSBs (as well as oxidized bases or abasic (apurinic/apyrimidinic, AP) sites).[44]”
BackgroundStructure-specific nucleases in genome dynamics and strategies for targeting cancers
Sun, H., Luo, M., Zhou, M., Zheng, L., Li, H., Esworthy, R. S., & Shen, B. (2024) · Journal of Molecular Cell Biology · doi:10.1093/jmcb/mjae019 · Cited by 3
“Given that a single unrepaired DSB may cause cell death (Bennett et al., 1993 , 1996 ), most chemotherapies also target replication forks to directly or indirectly induce DNA DSBs (Cannan and Pederson, 2016 ).”
Kler, A., Fok, M., Grundy, G. J., Sciacovelli, M., Dunn, W. B., & Vimalachandran, D. (2025) · Metabolomics · doi:10.1007/s11306-025-02319-y · Cited by 3
“Subsequently, this reduces concentrations of reactive oxygen species (ROS), a typical by-product of radiotherapy/radiation treatment that causes harmful double-stranded DNA (dsDNA) breaks (Cannan & Pederson, 2016 ).”
Metadata
- Authors
- Cannan, W. J., & Pederson, D. S.
- Affiliations
- University of Vermont (US)
- Corresponding author
- Pederson, David S.
- ORCID
- Cannan, Wendy J.
- Venue
- Journal of Cellular Physiology
- Publisher
- Wiley
- Published
- 2015-09-28
- Volume
- 231
- Issue
- 1
- Pages
- 3-14
- ISSN
- 0021-9541 (ISSN-L)
- 1097-4652
- PMC
- PMC4994891
- OpenAlex
- W1783508367
- Cited by
- 499
- References
- 153
- Citations by year
- 2026: 46 · 2025: 70 · 2024: 92 · 2023: 60 · 2022: 51 · 2021: 63 · 2020: 57 · 2019: 29 · 2018: 14 · 2017: 7 · 2016: 8 · 2015: 1
- FWCI
- 0.97
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Cellular Physiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NCI (P01-CA098993)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- DNA double-strand breaks, chromatin, ionizing radiation, DNA damage mechanisms, DNA repair pathways, non-homologous end joining, homologous recombination, mutational burden, loss of heterozygosity, chromosomal rearrangements, nucleosome, chromatin structure, cell cycle, replication fork stalling, chromothripsis, chromosome coiling
- MeSH terms
- Animals, Cell Cycle, Chromatin, DNA Repair, Humans, Radiation, Ionizing, DNA Breaks, Double-Stranded, DNA End-Joining Repair
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