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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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Cites
Crystal structure of the nucleosome core particle at 2.8 Å resolution
Luger, K., Mäder, A. W., Richmond, R. K., Sargent, D. F., & Richmond, T. J. (1997) · Nature · doi:10.1038/38444 · Cited by 9,466 · cited 2×
“Finally, reactions between ROS and nucleosomal DNA are impeded by the discrete interactions between histones and the DNA backbone at every helical turn (Luger et al., 1997).”
BackgroundFriedberg, E. C., Walker, G. C., Siede, W., Wood, R. D., Schultz, R. A., & Ellenberger, T. (2005) · doi:10.1128/9781555816704 · Cited by 5,683
Über einen die Erzeugung und Verwandlung des Lichtes betreffenden heuristischen Gesichtspunkt
Einstein, A. (1905) · Annalen der Physik · doi:10.1002/andp.19053220607 · Cited by 3,090
ATM and ATR Substrate Analysis Reveals Extensive Protein Networks Responsive to DNA Damage
Matsuoka, S., Ballif, B. A., Smogorzewska, A., McDonald, E. R., Hurov, K. E., Luo, J., Bakalarski, C. E., Zhao, Z., Solimini, N., Lerenthal, Y., et al. (2007) · Science · doi:10.1126/science.1140321 · Cited by 3,075
The mechanism of double-strand DNA break repair by the nonhomologous DNA end-joining pathway
Lieber, M. R. (2010) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.052308.093131 · Cited by 2,882 · cited 1×
“There are several excellent, recent reviews of DSB repair for readers looking for more detailed expositions (e.g., San Filippo et al., 2008; Lieber, 2010; Polo and Jackson, 2011; Asaithamby and Chen, 2011; Thompson, 2012; Mehta and Haber, 2014).”
BackgroundSupercoiling of the DNA template during transcription.
Liu, L. F., & Wang, J. C. (1987) · Proceedings of the National Academy of Sciences of the United States of America · doi:10.1073/pnas.84.20.7024 · Cited by 1,877 · cited 1×
“However, transcription elongation may occasionally outpace the action of topoisomerases, resulting in a transient accumulation of positive superhelical density ahead of the RNA polymerase, and a corresponding accumulation of negative superhelical density in the trailing region (Liu and Wang, 1987).”
BackgroundMechanism of Eukaryotic Homologous Recombination
Filippo, J. S., Sung, P., & Klein, H. L. (2008) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.77.061306.125255 · Cited by 1,766
Rate of depurination of native deoxyribonucleic acid
Lindahl, T. L., & Nyberg, B. (1972) · Biochemistry · doi:10.1021/bi00769a018 · Cited by 1,558 · cited 1×
“Most of these endogenously-generated ROS are neutralized, but enough escape to generate roughly 10,000 oxidative base lesions and another 10,000 base loss events per cell per day (Lindahl and Nyberg, 1972; Fraga et al., 1990 and reviewed in Friedberg et al., 2005).”
BackgroundWard, J. F. (1988) · Progress in nucleic acid research and molecular biology · doi:10.1016/s0079-6603(08)60611-x · Cited by 1,499
Spheroid Chromatin Units (ν Bodies)
Olins, A. L., & Olins, D. E. (1974) · Science · doi:10.1126/science.183.4122.330 · Cited by 1,430
Krokan, H. E., & Bjoras, M. (2013) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a012583 · Cited by 1,322
Solenoidal model for superstructure in chromatin.
Finch, J. T., & Klug, A. (1976) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.73.6.1897 · Cited by 1,256 · cited 2×
“Chromatin associated with transcriptionally active regions is generally in a relatively “open” or extended configuration, commonly referred to as a 10nm filament (orfiber) (Olins andOlins, 1974;Oudet et al., 1975; Finch and Klug, 1976; Woodcock et al., 1976).”
BackgroundBase-excision repair of oxidative DNA damage
David, S. S., O'Shea, V. L., & Kundu, S. (2007) · Nature · doi:10.1038/nature05978 · Cited by 1,238 · cited 1×
“Most such lesions are subject to base excision repair (BER), which entails production of gapped repair intermediates (for reviews, see David et al., 2007; Hegde et al., 2008; Robertson et al., 2009; Duclos et al., 2012; Krokan and Bjoras, 2013; Wallace, 2014).”
BackgroundDNA breaks and chromosome pulverization from errors in mitosis
Crasta, K., Ganem, N. J., Dagher, R., Lantermann, A. B., Ivanova, E. V., Pan, Y., Nezi, L., Protopopov, A., Chowdhury, D., & Pellman, D. (2012) · Nature · doi:10.1038/nature10802 · Cited by 1,227 · cited 1×
“Thus pulverization and rearrangement may occur over multiple cell divisions, until the damaged, rearranged chromosome, or fragments thereof, are taken up by the nucleus (Crasta et al., 2012).”
BackgroundStructure of the Ku heterodimer bound to DNA and its implications for double-strand break repair
Walker, J. R., Corpina, R. A., & Goldberg, J. D. (2001) · Nature · doi:10.1038/35088000 · Cited by 1,216 · cited 1×
“Ku heterodimers exist as preformed rings that encircle 3–4 bp of DNA, fitting along the contours of themajor andminor grooves (Walker et al., 2001).”
BackgroundOxidative damage to DNA during aging: 8-hydroxy-2'-deoxyguanosine in rat organ DNA and urine.
Fraga, C. G., Shigenaga, M. K., Park, J. W., Degan, P., & Ames, B. N. (1990) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.87.12.4533 · Cited by 1,106 · cited 1×
“Most of these endogenously-generated ROS are neutralized, but enough escape to generate roughly 10,000 oxidative base lesions and another 10,000 base loss events per cell per day (Lindahl and Nyberg, 1972; Fraga et al., 1990 and reviewed in Friedberg et al., 2005).”
BackgroundEndogenous DNA damage in humans: a review of quantitative data
Bont, R. D. (2004) · Mutagenesis · doi:10.1093/mutage/geh025 · Cited by 1,099
Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications
Polo, S. E., & Jackson, S. P. (2011) · Genes & Development · doi:10.1101/gad.2021311 · Cited by 1,092
Electron microscopic and biochemical evidence that chromatin structure is a repeating unit
Oudet, P., Gross-Bellard, M., & Chambon, P. (1975) · Cell · doi:10.1016/0092-8674(75)90149-x · Cited by 974
Etoposide: four decades of development of a topoisomerase II inhibitor
Hande, K. R. (1998) · European Journal of Cancer · doi:10.1016/s0959-8049(98)00228-7 · Cited by 962 · cited 1×
“Camptothecins are topoisomerase I inhibitors, while etoposides are topoisomerase II inhibitors (Hande, 1998; Koster et al., 2007).”
BackgroundSequence periodicities in chicken nucleosome core DNA
Satchwell, S. C., Drew, H. R., & TRAVERS, A. A. (1986) · Journal of Molecular Biology · doi:10.1016/0022-2836(86)90452-3 · Cited by 929
Sources of DNA Double-Strand Breaks and Models of Recombinational DNA RepairPreprint
Mehta, A., & Haber, J. E. (2014) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a016428 · Cited by 792 · cited 3×
“This frequency could account for the estimated 10–50 DSBs that form every day in every nucleated human cell (Vilenchik and Knudson, 2003; and reviewed in Mehta and Haber, 2014), but only if SSBs persist for a large fraction of the cell cycle.”
BackgroundThe Human Transcriptome Map: Clustering of Highly Expressed Genes in Chromosomal Domains
Caron, H. N., van Schaik, B. D. C., van der Mee, M., Baas, F., Riggins, G. J., Sluis, P. V., Hermus, M.-C., van Asperen, R., Boon, K., Voûte, P. A., et al. (2001) · Science · doi:10.1126/science.1056794 · Cited by 730 · cited 1×
““Regions of increased gene expression,” or RIDGEs (Caron et al., 2001; Versteeg et al., 2003), reside within euchromatic regions.”
BackgroundEndogenous DNA double-strand breaks: production, fidelity of repair, and induction of cancer
Vilenchik, M. M., & Knudson, A. G. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2135498100 · Cited by 717
DNA bending and its relation to nucleosome positioning
Drew, H. R., & TRAVERS, A. A. (1985) · Journal of Molecular Biology · doi:10.1016/0022-2836(85)90396-1 · Cited by 706 · cited 1×
“First, most DNA segments adopt a discrete helical orientation when bent, either free in space or when wrapped about a histone octamer (Drew and Travers, 1985; Satchwell et al., 1986).”
BackgroundRobertson, A. B., Klungland, A., Rognes, T., & Leiros, I. (2009) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-009-8736-z · Cited by 685 · cited 1×
“Most such lesions are subject to base excision repair (BER), which entails production of gapped repair intermediates (for reviews, see David et al., 2007; Hegde et al., 2008; Robertson et al., 2009; Duclos et al., 2012; Krokan and Bjoras, 2013; Wallace, 2014).”
BackgroundEarly steps in the DNA base excision/single-strand interruption repair pathway in mammalian cells
Hegde, M. L., Hazra, T. K., & MITRA, S. P. (2008) · Cell Research · doi:10.1038/cr.2008.8 · Cited by 679 · cited 1×
“Most such lesions are subject to base excision repair (BER), which entails production of gapped repair intermediates (for reviews, see David et al., 2007; Hegde et al., 2008; Robertson et al., 2009; Duclos et al., 2012; Krokan and Bjoras, 2013; Wallace, 2014).”
BackgroundBleomycins: towards better therapeutics
Chen, J., & Stubbe, J. (2005) · Nature reviews. Cancer · doi:10.1038/nrc1547 · Cited by 668 · cited 1×
“Although bleomycin carries just one reactive moiety, it somehow produces about one DSB for every 10 single-strand breaks it generates (Povirk, 1996; Chen and Stubbe, 2005).”
BackgroundTruong, L. N., Li, Y., Shi, L. Z., Hwang, P. Y.-H., He, J. N., Wang, H., Razavian, N. B., Berns, M. W., & Wu, X. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1213431110 · Cited by 570
Balasubramanian, B., Pogozelski, W. K., & Tullius, T. D. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.17.9738 · Cited by 560
CtIP-BRCA1 modulates the choice of DNA double-strand-break repair pathway throughout the cell cycle
Yun, M. H., & Hiom, K. (2009) · Nature · doi:10.1038/nature07955 · Cited by 556 · cited 1×
“Tyrosyl-DNA phosphodiesterase, for example, can require several hours to remove phosphoglycolate moieties from 3’ DNA ends (Zhou et al., 2009).”
BackgroundChanges in chromatin structure and mobility in living cells at sites of DNA double-strand breaks
Kruhlak, M. J., Celeste, A., Dellaire, G., Fernandez-Capetillo, O., Müller, W. G., McNally, J. G., Bazett-Jones, D. P., & Nussenzweig, A. (2006) · The Journal of Cell Biology · doi:10.1083/jcb.200510015 · Cited by 518 · cited 1×
“Indeed, DSB repair may not occur at all until heterochromatin decondenses (Kruhlak et al., 2006; Lorat et al., 2012).”
BackgroundCDK targets Sae2 to control DNA-end resection and homologous recombination
Huertas, P., Cortés‐Ledesma, F., Sartori, A. A., Aguilera, A., & Jackson, S. P. (2008) · Nature · doi:10.1038/nature07215 · Cited by 509 · cited 4×
“However, the processing of DNA ends that form hairpins or are attached to proteins requires additional help from the endonuclease Sae2/Ctp1/CtIP.”
BackgroundInfluentialMechanisms of DNA double-strand break repair and their potential to induce chromosomal aberrations
Pfeiffer, P. (2000) · Mutagenesis · doi:10.1093/mutage/15.4.289 · Cited by 489
Replication fork stalling at natural impediments
Mirkin, E. V., & Mirkin, S. M. (2007) · Microbiology and Molecular Biology Reviews · doi:10.1128/mmbr.00030-06 · Cited by 482 · cited 1×
“…structures, bulky lesions, polymerase blocking oxidative lesions, abasic sites, chemical or IR-generated inter-strand crosslinks, or as a result of collisions with transcription complexes and certain DNA binding proteins (Prado and Aguilera, 2005; Mirkin and Mirkin, 2007; Dextraze et al., 2010).”
BackgroundClustered DNA damages induced in isolated DNA and in human cells by low doses of ionizing radiation
Sutherland, B. M., Bennett, P. V., Sidorkina, O. M., & Laval, J. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.97.1.103 · Cited by 473
Povirk, L. F. (1996) · Mutation research. Fundamental and molecular mechanisms of mutagenesis · doi:10.1016/0027-5107(96)00023-1 · Cited by 432
Mating-Type Genes and MAT Switching in Saccharomyces cerevisiae
Haber, J. E. (2012) · Genetics · doi:10.1534/genetics.111.134577 · Cited by 424 · cited 2×
“…occurs during the development of somatic nuclei in protozoans (reviewed in Duharcourt et al., 2009), mating-type switching in yeast (reviewed in Haber, 2012), T-cell receptor formation in T-lymphocytes, and immunoglobulin class switching in B-lymphocytes (reviewed in Soulas-Sprauel et al.,…”
BackgroundInitiation of Meiotic Recombination: How and Where? Conservation and Specificities Among Eukaryotes
de Massy, B. (2013) · Annual Review of Genetics · doi:10.1146/annurev-genet-110711-155423 · Cited by 407
Proteome-wide identification of in vivo targets of DNA damage checkpoint kinases
Smolka, M. B., Albuquerque, C. P., Chen, S.-H., & Zhou, H. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0701622104 · Cited by 404
Base excision repair: A critical player in many games
Wallace, S. S. (2014) · DNA Repair · doi:10.1016/j.dnarep.2014.03.030 · Cited by 401 · cited 1×
“Most such lesions are subject to base excision repair (BER), which entails production of gapped repair intermediates (for reviews, see David et al., 2007; Hegde et al., 2008; Robertson et al., 2009; Duclos et al., 2012; Krokan and Bjoras, 2013; Wallace, 2014).”
BackgroundChromothripsis and cancer: causes and consequences of chromosome shattering
Forment, J. V., Kaidi, A., & Jackson, S. P. (2012) · Nature reviews. Cancer · doi:10.1038/nrc3352 · Cited by 393 · cited 1×
“In chromothripsis (“chromosome shattering”), the chromosome rearrangement and deletion events can number in the hundreds, but are usually confined to a single chromosome (reviewed in Forment et al., 2012).”
BackgroundAn update on PARP inhibitors—moving to the adjuvant setting
Sonnenblick, A., de Azambuja, E., Azim, H. A., & Piccart, M. J. (2014) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2014.163 · Cited by 390
Higher-Order Structures of Chromatin: The Elusive 30 nm Fiber
Tremethick, D. J. (2007) · Cell · doi:10.1016/j.cell.2007.02.008 · Cited by 368
Little, M. P., Azizova, T. V., Bazyka, D., Bouffler, S. D., Cardis, E., Chekin, S., Chumak, V. V., Cucinotta, F. A., de Vathaire, F., Hall, P., et al. (2012) · Environmental Health Perspectives · doi:10.1289/ehp.1204982 · Cited by 367 · cited 1×
“For example, cardiovascular disease may increase mortality following radiation exposure (Little et al., 2012).”
BackgroundThompson, L. H. (2012) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2012.06.002 · Cited by 357
The structure of DNA in a nucleosome.
Hayes, J. J., Tullius, T. D., & Wolffe, A. P. (1990) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.87.19.7405 · Cited by 354 · cited 1×
“Thus, the overall extent to which nucleosomes mask ROS-reactive moieties in DNA is modest, although one commonly sees a 10 bp periodicity in ROS reactivity, which matches the helical repeat of DNA in nucleosomes (Hayes et al., 1990; Franchet-Beuzit et al., 1993).”
BackgroundVersteeg, R., van Schaik, B. D. C., van Batenburg, M. F., Roos, M., Monajemi, R., Caron, H. N., Bussemaker, H. J., & van Kampen, A. H. C. (2003) · Genome Research · doi:10.1101/gr.1649303 · Cited by 351 · cited 1×
“This frequency could account for the estimated 10–50 DSBs that form every day in every nucleated human cell (Vilenchik and Knudson, 2003; and reviewed in Mehta and Haber, 2014), but only if SSBs persist for a large fraction of the cell cycle.”
BackgroundCHROMOSOME ABERRATIONS INDUCED BY X-RAYS
Sax, K. (1938) · Genetics · doi:10.1093/genetics/23.5.494 · Cited by 345
DNA damage signaling in response to double-strand breaks during mitosis
Giunta, S., Belotserkovskaya, R., & Jackson, S. P. (2010) · The Journal of Cell Biology · doi:10.1083/jcb.200911156 · Cited by 325 · cited 1×
“At that point, the incompletely replicated chromosomewill trigger a DNAdamage response, butone thatmaydecaybefore replication is complete (Giunta et al., 2010; van Vugt et al., 2010).”
BackgroundAntitumour drugs impede DNA uncoiling by topoisomerase I
Koster, D. A., Palle, K., Bot, E. S. M., Bjornsti, M., & Dekker, N. H. (2007) · Nature · doi:10.1038/nature05938 · Cited by 299
Impairment of replication fork progression mediates RNA polII transcription‐associated recombination
Prado, F., & Aguilera, A. (2005) · The EMBO Journal · doi:10.1038/sj.emboj.7600602 · Cited by 294
Effects of Radiations of Different Qualities on Cells: Molecular Mechanisms of Damage and Repair
GOODHEAD, D. T., Thacker, J., & Cox, R. (1993) · International Journal of Radiation Biology · doi:10.1080/09553009314450721 · Cited by 293 · cited 1×
“Low or high LET radiation doses as low as 1 Gray (100 rad) can produce clustered lesions (Goodhead et al., 1993; Rydberg, 1996; Sutherland et al., 2000a), and Monte Carlo-based modeling of radiation tracks suggests that low and high LET radiation can generate, respectively, up to 10 and 25 lesions…”
BackgroundTang, H. L., Tang, H. M., Mak, K. H., Hu, S., Wang, S. S., Wong, K. M., Wong, C. S. T., Wu, H. Y., Law, H. T., Liu, K., et al. (2012) · Molecular Biology of the Cell · doi:10.1091/mbc.e11-11-0926 · Cited by 293
Hinton, J. A., & Hofmann, W. (2009) · Annual Review of Astronomy and Astrophysics · doi:10.1146/annurev-astro-082708-101816 · Cited by 291 · cited 1×
“The resulting cascade of ionized particles and photons, known as an air shower, can be many km wide (Hinton and Hofmann, 2009).”
BackgroundHeterochromatin is refractory to γ-H2AX modification in yeast and mammals
Kim, J., Kruhlak, M. J., Dotiwala, F., Nussenzweig, A., & Haber, J. E. (2007) · The Journal of Cell Biology · doi:10.1083/jcb.200612031 · Cited by 276 · cited 1×
“A related challenge is the apparent suppression of g-H2AX foci formation in heterochromatin (Kim et al., 2007) and the correspondingly slow repairofDSBs in heterochromatin (Slijepcevic andNatarajan, 1994; reviewed in Falk et al., 2010).”
BackgroundHamperl, S., & Cimprich, K. A. (2014) · DNA repair · doi:10.1016/j.dnarep.2014.03.023 · Cited by 275 · cited 2×
“Consistent with this prediction, defects in certain RNA processing enzymes produce hyper-recombination phenotypes can be suppressed by overexpression of RNase H (reviewed in Hamperl and Cimprich, 2014).”
BackgroundDelayed repair of radiation induced clustered DNA damage: Friend or foe?
Eccles, L. J., O’Neill, P., & Lomax, M. E. (2010) · Mutation research. Fundamental and molecular mechanisms of mutagenesis · doi:10.1016/j.mrfmmm.2010.11.003 · Cited by 245 · cited 1×
“BER-dependent formation of DSBs has been observed in multiple in vitro studies (for reviews, see Eccles et al., 2011; Sage and Harrison, 2011) and now forms the basis for assays to measure the abundance of non-strand break clustered damages (Sutherland et al., 2000b; Sutherland et al., 2003).”
BackgroundClustered DNA lesion repair in eukaryotes: Relevance to mutagenesis and cell survival
Sage, É., & Harrison, L. (2010) · Mutation research. Fundamental and molecular mechanisms of mutagenesis · doi:10.1016/j.mrfmmm.2010.12.010 · Cited by 238
Nucleases and helicases take center stage in homologous recombination
Mimitou, E. P., & Symington, L. S. (2009) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2009.01.010 · Cited by 238 · cited 1×
“Acting together, MRE11 and CtIP remove 5’ strands in 50–100NT increments (reviewed in Mimitou and Symington, 2009).”
Backgroundvan Vugt, M. A. T. M., Gardino, A. K., Linding, R., Ostheimer, G. J., Reinhardt, H. C., Ong, S.-E., Tan, C. S. H., Miao, H., Keezer, S. M., Li, J., et al. (2010) · PLoS Biology · doi:10.1371/journal.pbio.1000287 · Cited by 236
Non-random distribution of DNA double-strand breaks induced by particle irradiation
LOBRICH, P. K. C. A. B. R. M. (1996) · International Journal of Radiation Biology · doi:10.1080/095530096144680 · Cited by 232 · cited 1×
“High LET a particles and heavy ions travel along straight tracks and exhibit far higher collision rates, producing DSB patterns that appear to be non-random (Lobrich et al., 1996; Prise et al., 2001; Rydberg, 2001).”
BackgroundRydberg, B., & Rydberg, B. (1996) · Radiation Research · doi:10.2307/3579175 · Cited by 230 · cited 1×
“Low or high LET radiation doses as low as 1 Gray (100 rad) can produce clustered lesions (Goodhead et al., 1993; Rydberg, 1996; Sutherland et al., 2000a), and Monte Carlo-based modeling of radiation tracks suggests that low and high LET radiation can generate, respectively, up to 10 and 25 lesions…”
BackgroundStructural repeating units in chromatin
Woodcock, C. L. F., Safer, J. P., & Stanchfield, J. E. (1976) · Experimental Cell Research · doi:10.1016/0014-4827(76)90659-5 · Cited by 228
Sutherland, B. M., Bennett, P. V., Sidorkina, O. M., & Laval, J. (2000) · Biochemistry · doi:10.1021/bi9927989 · Cited by 227
An impenetrable barrier to ultrarelativistic electrons in the Van Allen radiation belts
Baker, D. N., Jaynes, A. N., Hoxie, V. C., Thorne, R. M., Foster, J. C., Li, X., Fennell, J. F., Wygant, J. R., Kanekal, S. G., Erickson, P. J., et al. (2014) · Nature · doi:10.1038/nature13956 · Cited by 224
Ionizing radiation biomarkers for potential use in epidemiological studies
Pernot, E., Hall, J. A., Baatout, S., Benotmane, M. A., Blanchardon, E., Bouffler, S. D., Saghire, H. E., Gomolka, M., Guertler, A., Harms‐Ringdahl, M., et al. (2012) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2012.05.003 · Cited by 215
Abortive base-excision repair of radiation-induced clustered DNA lesions in Escherichia coli
Blaisdell, J. O., & Wallace, S. S. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.131077798 · Cited by 209
Higher order coiling of DNA in chromatin
Worcel, A., & Benyajati, C. (1977) · Cell · doi:10.1016/0092-8674(77)90187-8 · Cited by 202 · cited 1×
“10 nm chromatin fibers can coil to produce more compact, 30 nm filaments that, generally, are transcriptionally inactive (Pooley et al., 1974; Finch and Klug, 1976; Olins and Olins, 1979; Ris and Kubai, 1970; Worcel and Benyajati, 1977).”
BackgroundChromatin structure influences the sensitivity of DNA to γ-radiation
Falk, M., Lukášová, E., & Kozubek, S. (2008) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2008.07.010 · Cited by 196 · cited 1×
“Oneof themost compelling studies on the vulnerability of transcriptionally active chromatin to DSB formation combined use of g-H2AX immunofluorescence with Immuno-FISH, to quantify IR-induced DSBs in individual chromosomes (Falk et al., 2008).”
MethodA Review of Studies of Ionizing Radiation-Induced Double-Strand Break Clustering
Prise, K. M., Pinto, M., Newman, H. C., & Michael, B. D. (2001) · Radiation Research · doi:10.1667/0033-7587(2001)156[0572:arosoi]2.0.co;2 · Cited by 196
Break-induced replication: functions and molecular mechanism
Malkova, A., & Ira, G. (2013) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2013.05.007 · Cited by 192
A Fast Monte Carlo Algorithm to Simulate the Spectrum of DNA Damages Formed by Ionizing Radiation
Semenenko, V. A., & Stewart, R. D. (2004) · Radiation Research · doi:10.1667/rr3140 · Cited by 190
Wahba, L., Gore, S. K., & Koshland, D. E. (2013) · eLife · doi:10.7554/elife.00505 · Cited by 188
Ris, H., & Kubai, D. F. (1970) · Annual Review of Genetics · doi:10.1146/annurev.ge.04.120170.001403 · Cited by 184
Soulas-Sprauel, P., Rivera-Muñoz, P., Malivert, L., Guyader, G. L., Abramowski, V., Revy, P., & de Villartay, J. (2007) · Oncogene · doi:10.1038/sj.onc.1210875 · Cited by 180
Yang, N.-J., Galick, H., & Wallace, S. (2004) · DNA Repair · doi:10.1016/j.dnarep.2004.04.014 · Cited by 175
Chromosomes without a 30-nm chromatin fiber
Joti, Y., Hikima, T., Nishino, Y., Kamada, F., Hihara, S., Takata, H., Ishikawa, T., & Maeshima, K. (2012) · Nucleus · doi:10.4161/nucl.21222 · Cited by 172 · cited 1×
“…of higher order chromatin would take us beyond the scope of this review, but interested readers may wish to consult one or more of the recent reviews of the subject (van Holde and Zlatanova, 2007; Tremethick, 2007; Mozziconacci and Lavelle, 2009; Grigoryev and Woodcock, 2012; Joti et al., 2012).”
BackgroundLinker histones H1 and H5 prevent the mobility of positioned nucleosomes.
Pennings, S., Meersseman, G., & Bradbury, E. M. (1994) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.91.22.10275 · Cited by 171
Wellinger, R. E., Prado, F., & Aguilera, A. (2006) · Molecular and Cellular Biology · doi:10.1128/mcb.26.8.3327-3334.2006 · Cited by 171
The Three-Dimensional Structure of Human Interphase Chromosomes Is Related to the Transcriptome Map
Götze, S., Langerak, J. M., Gierman, H. J., de Leeuw, W. C., Giromus, O., Indemans, M. H. G., Köster, J., Ondřej, V., Versteeg, R., & DRIEL, R. V. (2007) · Molecular and Cellular Biology · doi:10.1128/mcb.00208-07 · Cited by 162 · cited 1×
“The chromatin within these regions is in a relatively open configuration (Goetze et al., 2007).”
BackgroundChromothripsis and Human Disease: Piecing Together the Shattering Process
Maher, C. A., & Wilson, R. K. (2012) · Cell · doi:10.1016/j.cell.2012.01.006 · Cited by 159 · cited 1×
“Other distinguishing features of chromothripsis include a low gene copy number within shattered regions, and alternations between retained heterozygosity and loss of heterozygosity (Maher and Wilson, 2012).”
Asaithamby, A., & Chen, D. J. (2010) · Mutation research. Fundamental and molecular mechanisms of mutagenesis · doi:10.1016/j.mrfmmm.2010.11.002 · Cited by 156 · cited 1×
“There are several excellent, recent reviews of DSB repair for readers looking for more detailed expositions (e.g., San Filippo et al., 2008; Lieber, 2010; Polo and Jackson, 2011; Asaithamby and Chen, 2011; Thompson, 2012; Mehta and Haber, 2014).”
BackgroundChromatin organization — The 30nm fiber
Grigoryev, S. A., & Woodcock, C. L. F. (2012) · Experimental Cell Research · doi:10.1016/j.yexcr.2012.02.014 · Cited by 153 · cited 1×
“…of higher order chromatin would take us beyond the scope of this review, but interested readers may wish to consult one or more of the recent reviews of the subject (van Holde and Zlatanova, 2007; Tremethick, 2007; Mozziconacci and Lavelle, 2009; Grigoryev and Woodcock, 2012; Joti et al., 2012).”
BackgroundTichy, E. D., Pillai, R., Deng, L., Liang, L., Tischfield, J., Schwemberger, S. J., Babcock, G. F., & Stambrook, P. J. (2010) · Stem Cells and Development · doi:10.1089/scd.2010.0058 · Cited by 152
Mutations Arising During Repair of Chromosome Breaks
Malkova, A., & Haber, J. E. (2012) · Annual Review of Genetics · doi:10.1146/annurev-genet-110711-155547 · Cited by 147 · cited 13×
“In addition to checkpoint control-related mechanisms, the choice of HRR over NHEJ in S and G2 phases is influenced by the cell cycle-dependent, activating phosphorylation of the resection factor Sae2 (Huertas et al., 2008).”
BackgroundInfluentialHigher-order chromatin structure in DSB induction, repair and misrepair
Falk, M., Lukášová, E., & Kozubek, S. (2010) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2010.01.013 · Cited by 137 · cited 1×
“A related challenge is the apparent suppression of g-H2AX foci formation in heterochromatin (Kim et al., 2007) and the correspondingly slow repairofDSBs in heterochromatin (Slijepcevic andNatarajan, 1994; reviewed in Falk et al., 2010).”
BackgroundActivation of DSB Processing Requires Phosphorylation of CtIP by ATR
Peterson, S., Li, Y., Wu-Baer, F., Chait, B. T., Baer, R. J., Yan, H., Gottesman, M. E., & Gautier, J. (2012) · Molecular Cell · doi:10.1016/j.molcel.2012.11.020 · Cited by 137
Reynolds, P., Anderson, J. A., Harper, J. V., Hill, M. A., Botchway, S. W., Parker, A. W., & O’Neill, P. (2012) · Nucleic Acids Research · doi:10.1093/nar/gks879 · Cited by 134
Complex regulation and function of activation-induced cytidine deaminase
Stavnezer, J. (2011) · Trends in Immunology · doi:10.1016/j.it.2011.03.003 · Cited by 133
Langmore, J., & Paulson, J. R. (1983) · The Journal of Cell Biology · doi:10.1083/jcb.96.4.1120 · Cited by 127 · cited 1×
“…30-40 nm (reflecting side-by-side packing of 30 nm chromatin filaments), 11 and 6 nm (reflecting the packing constraints of individual nucleosomes), and 2.1 and 2.7 nm (reflecting thediameter ofDNAand its pitchwithin nucleosomes, respectively) (Langmore and Paulson, 1983, and references therein).”
BackgroundInfluentialKnock-In Reporter Mice Demonstrate that DNA Repair by Non-homologous End Joining Declines with Age
Vaidya, A. M., Mao, Z., Tian, X., Spencer, B., Seluanov, A., & Gorbunova, V. A. (2014) · PLoS Genetics · doi:10.1371/journal.pgen.1004511 · Cited by 125
32. E. Heitz: Heterochromatin, Chromocentren, Chromomeren
(1929) · Berichte der Deutschen Botanischen Gesellschaft · doi:10.1111/j.1438-8677.1929.tb01609.x · Cited by 125
Yang, N., Chaudhry, M. A., & Wallace, S. S. (2005) · DNA repair · doi:10.1016/j.dnarep.2005.07.003 · Cited by 119 · cited 1×
“There is compelling evidence that BER-driven DSB formation also occurs in vivo, in both prokaryotes and eukaryotes (Blaisdell andWallace, 2001; Blaisdell et al., 2001; Yang et al., 2004; Yang et al., 2006).”
BackgroundBase Excision Repair Processing of Radiation-induced Clustered DNA Lesions
Blaisdell, J. O., Harrison, L., & Wallace, S. S. (2001) · Radiation Protection Dosimetry · doi:10.1093/oxfordjournals.rpd.a006634 · Cited by 119 · cited 1×
“There is compelling evidence that BER-driven DSB formation also occurs in vivo, in both prokaryotes and eukaryotes (Blaisdell andWallace, 2001; Blaisdell et al., 2001; Yang et al., 2004; Yang et al., 2006).”
BackgroundDahm-Daphi, C. S. J. (2000) · International Journal of Radiation Biology · doi:10.1080/095530000139023 · Cited by 115 · cited 3×
“Ye Y, Stahley MR, Xu J, Friedman JI, Sun Y, McKnight JN, Gray JJ, Bowman GD, Stivers JT. 2012.”
BackgroundCancer Genomes Evolve by Pulverizing Single Chromosomes
Meyerson, M., & Pellman, D. (2011) · Cell · doi:10.1016/j.cell.2010.12.025 · Cited by 115
Rydberg, B., Holley, W. R., Mian, S. I., & Chatterjee, A. (1998) · Journal of Molecular Biology · doi:10.1006/jmbi.1998.2150 · Cited by 114
Rules of engagement for base excision repair in chromatin
Odell, I. D., Wallace, S. S., & Pederson, D. S. (2012) · Journal of Cellular Physiology · doi:10.1002/jcp.24134 · Cited by 113
Self-citationChromatin fiber structure: Where is the problem now?
van Holde, K. E., & Zlatanova, J. S. (2007) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2007.08.005 · Cited by 106
Hypersensitivity of DNA in transcriptionally active chromatin to ionizing radiation
Chiu, S., Oleinick, N. L., Friedman, L. R., & Stambrook, P. J. (1982) · Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression · doi:10.1016/0167-4781(82)90166-x · Cited by 104 · cited 1×
“By combining pulsed field gel electrophoresis with Southern blotting, (Chiu et al., 1982) were able to show that housekeeping genes aremore vulnerable to IR-inducedDSBs thana-satelliteorbulkDNA.”
MethodSystematic Review: Charged-Particle Radiation Therapy for Cancer
Terasawa, T., Dvorak, T., Ip, S., Raman, G., Lau, J., & Trikalinos, T. A. (2009) · Annals of Internal Medicine · doi:10.7326/0003-4819-151-8-200910200-00145 · Cited by 104
Colnaghi, R., Carpenter, G., Volker, M., & O’Driscoll, M. (2011) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2011.07.010 · Cited by 101 · cited 1×
“This sets the stage for another round of NHEJ that restores the dicentric chromosome, allowing the breakage-fusion cycle to repeat (Colnaghi et al., 2011; Meyerson and Pellman, 2011).”
BackgroundWeinfeld, M., & Soderlind, K. J. M. (1991) · Biochemistry · doi:10.1021/bi00218a031 · Cited by 98
Rodriguez, Y., & Smerdon, M. J. (2013) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.441444 · Cited by 98
Polyamine-nucleic acid interactions and the effects on structure in oriented DNA fibers
van Dam, L. (2002) · Nucleic Acids Research · doi:10.1093/nar/30.2.419 · Cited by 97
The complexity of DNA double strand breaks is a critical factor enhancing end-resection
Yajima, H., Fujisawa, H., Nakajima, N. I., Hirakawa, H., Jeggo, P. A., Okayasu, R., & Fujimori, A. (2013) · DNA repair · doi:10.1016/j.dnarep.2013.08.009 · Cited by 93
DNA end resection is needed for the repair of complex lesions in G1-phase human cells
Averbeck, N., Ringel, O., Herrlitz, M., Jakob, B., Durante, M., & Taucher-Scholz, G. (2014) · Cell Cycle · doi:10.4161/15384101.2015.941743 · Cited by 92 · cited 1×
“It appears, however, that CtIP and other end resection factors can be recruited to complexDSBs in G1 phase (Yajima et al., 2013; Averbeck et al., 2014) where, presumably, they initiate MMEJ-mediated repair of complex damages.”
BackgroundHeterochromatin and chromosome aberrations
Natarajan, A. T., & Ahnstr�m, G. (1969) · Chromosoma · doi:10.1007/bf00325989 · Cited by 91
Galactic cosmic ray composition and energy spectra
Mewaldt, R. A. (1994) · Advances in Space Research · doi:10.1016/0273-1177(94)90536-3 · Cited by 88 · cited 1×
“The remaining 1% are high-Z, high-energy (HZE) atomic nuclei, derived from heavier elements (Mewaldt, 1994; NASA, 2006).”
BackgroundRadioprotection of DNA by Polyamines
Spotheim-Maurizot, M., Ruiz, S., Sabattier, R., & Charlier, M. (1995) · International Journal of Radiation Biology · doi:10.1080/09553009514551561 · Cited by 88
When catastrophe strikes a cell
Tubío, J. M. C., & Estivill, X. (2011) · Nature · doi:10.1038/470476a · Cited by 88
Franchet-Beuzit, J., Spotheim-Maurizot, M., Sabattier, R., Blazy, B., & Charlier, M. (1993) · Biochemistry · doi:10.1021/bi00059a031 · Cited by 87 · cited 2×
“Variations in groove width are sometimes sequence-directed, which may, for example, explain why 5’-AATT-3’ sequences are less sensitive than average to radiation-induced strand-breaks (Franchet-Beuzit et al., 1993; Sy JOURNAL OF CELLULAR PHYSIOLOGY et al., 1997).”
BackgroundDuharcourt, S., Lepère, G., & Meyer, É. (2009) · Trends in Genetics · doi:10.1016/j.tig.2009.05.007 · Cited by 85 · cited 1×
“Programmed formation of DSBs also occurs during the development of somatic nuclei in protozoans (reviewed in Duharcourt et al., 2009), mating-type switching in yeast (reviewed in Haber, 2012), T-cell receptor formation in T-lymphocytes, and immunoglobulin class switching in B-lymphocytes (reviewed…”
BackgroundSutherland, B. M., Georgakilas, A. G., Bennett, P. V., Laval, J., & Sutherland, J. C. (2003) · Mutation research. Fundamental and molecular mechanisms of mutagenesis · doi:10.1016/j.mrfmmm.2003.08.005 · Cited by 85
Zhou, T., Akopiants, K., Mohapatra, S., Lin, P.-S., Valerie, K. C., Ramsden, D. A., Lees‐Miller, S. P., & Povirk, L. F. (2009) · DNA repair · doi:10.1016/j.dnarep.2009.05.003 · Cited by 84 · cited 1×
“Tyrosyl-DNA phosphodiesterase, for example, can require several hours to remove phosphoglycolate moieties from 3’ DNA ends (Zhou et al., 2009).”
BackgroundThe shape of the radiation dose response for DNA double-strand break induction and repair
Barnard, S. G. R., Bouffler, S. D., & Rothkamm, K. (2013) · Genome Integrity · doi:10.1186/2041-9414-4-1 · Cited by 83
Prasad, A., Wallace, S. S., & Pederson, D. S. (2007) · Molecular and Cellular Biology · doi:10.1128/mcb.00791-07 · Cited by 83
Self-citationBase excision repair of 8-oxoG in dinucleosomes
Menoni, H., Shukla, M. S., Gerson, V., Dimitrov, S. I., & Angelov, D. (2011) · Nucleic Acids Research · doi:10.1093/nar/gkr761 · Cited by 81 · cited 1×
“…lesions are repaired varies bothwith the distance between the lesion and the edge of the nucleosome, and the lesion’s helical orientation relative to the underlying histoneoctamer (Odell et al., 2013; also, Menoni et al., 2012; Ye et al., 2012; Maher et al., 2013; Rodriguez and Smerdon, 2013).”
BackgroundTakahashi, T. S., Burguiere-Slezak, G., van der Kemp, P. A., & Boiteux, S. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1012582108 · Cited by 79
Chromatin structure and radiation-induced DNA damage: From structural biology to radiobiology
Lavelle, C., & Foray, N. (2014) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2014.01.012 · Cited by 70 · cited 1×
“Evidence of this includes studies in which the frequency of DSB formation increased after chromatin-associated proteins were stripped from DNA, using high salt (reviewed in Lavelle and Foray, 2014).”
BackgroundLorat, Y., Schanz, S., Schuler, N., Wennemuth, G., Rübe, C., & Rübe, C. E. (2012) · PLoS ONE · doi:10.1371/journal.pone.0038165 · Cited by 70 · cited 1×
“Indeed, DSB repair may not occur at all until heterochromatin decondenses (Kruhlak et al., 2006; Lorat et al., 2012).”
BackgroundEstimation of Yields of OH Radicals in Water Irradiated by Ionizing Radiation
Yamaguchi, H., Uchihori, Y., YASUDA, N., Takada, M., & Kitamura, H. (2005) · Journal of Radiation Research · doi:10.1269/jrr.46.333 · Cited by 70
Sequence-dependent variations of DNA structure modulate radiation-induced strand breakage
D. SY, C. S. (1997) · International Journal of Radiation Biology · doi:10.1080/095530097143365 · Cited by 70
Cannan, W. J., Tsang, B. P., Wallace, S. S., & Pederson, D. S. (2014) · Journal of Biological Chemistry · doi:10.1074/jbc.m114.571588 · Cited by 68 · cited 1×
“When tested however, nucleosomes suppressed DSB formation at clustered lesions far more than predicted (Cannan et al., 2014).”
BackgroundSelf-citationRecombination and ReplicationPreprint
Syeda, A. H., Hawkins, M., & McGlynn, P. (2014) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a016550 · Cited by 68
Radiation-induced DNA Damage and Chromatin Structure
Rydberg, B. (2001) · Acta Oncologica · doi:10.1080/02841860152619070 · Cited by 66
Radulescu, I., Elmroth, K., & Stenerlöw, B. (2004) · Radiation Research · doi:10.1667/rr3094 · Cited by 65
The relation between the unit thread of chromosomes and isolated nucleohistone
Pooley, A. S., Pardon, J. F., & Richards, B. M. (1974) · Journal of Molecular Biology · doi:10.1016/0022-2836(74)90314-3 · Cited by 64
The radiation hypersensitivity of cells at mitosis
Stobbe, C. C., Park, S. J., & Chapman, J. D. (2002) · International Journal of Radiation Biology · doi:10.1080/09553000210166570 · Cited by 64
Frankenberg-Schwager, M., Gebauer, A., Koppe, C., Wolf, H., Pralle, E., & Frankenberg, D. (2009) · Radiation Research · doi:10.1667/rr0784.1 · Cited by 63 · cited 1×
“This creates a substrate that, following removal of non-annealed DNA ends, is competent for gap filling and ligation (by DNA ligase IV in yeast and DNA ligase III in mammalian cells), as also occurs during single strand annealing repair (see Frankenberg-Schwager et al., 2009).”
BackgroundPinto, M., Prise, K. M., & Michael, B. D. (2005) · Radiation Research · doi:10.1667/rr3394 · Cited by 61
Modeling of ultrasoft X-ray induced DNA damage using structured higher order DNA targets
Bernhardt, P., Friedland, W., Jacob, P., & Paretzke, H. G. (2002) · International Journal of Mass Spectrometry · doi:10.1016/s1387-3806(02)00879-5 · Cited by 57 · cited 1×
“It also supports the use of IR-induced DSB patterns to determine nucleosome positions and investigate the structure of the 30 nm chromatin fiber (Rydberg et al., 1998; Rydberg, 2001; Bernhardt et al., 2003).”
MethodDNA interstrand cross-links induced by ionizing radiation: An unsung lesion
Dextraze, M.-E., Gantchev, T. G., Girouard, S., & Hunting, D. J. (2010) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2009.12.007 · Cited by 56 · cited 1×
“…structures, bulky lesions, polymerase blocking oxidative lesions, abasic sites, chemical or IR-generated inter-strand crosslinks, or as a result of collisions with transcription complexes and certain DNA binding proteins (Prado and Aguilera, 2005; Mirkin and Mirkin, 2007; Dextraze et al., 2010).”
BackgroundStereo electron microscopy of the 25-nm chromatin fibers in isolated nuclei.
Olins, A. L., & Olins, D. E. (1979) · The Journal of Cell Biology · doi:10.1083/jcb.81.1.260 · Cited by 56
Enzymatic Excision of Uracil Residues in Nucleosomes Depends on the Local DNA Structure and Dynamics
Ye, Y., Stahley, M. R., Xu, J., Friedman, J. I., Sun, Y., McKnight, J. N., Gray, J. J., Bowman, G. D., & Stivers, J. T. (2012) · Biochemistry · doi:10.1021/bi3006412 · Cited by 55
Energy deposition mechanisms and biochemical aspects of DNA strand breaks by ionizing radiation
Chatterjee, A., & Holley, W. R. (1991) · International Journal of Quantum Chemistry · doi:10.1002/qua.560390508 · Cited by 53 · cited 1×
“Although low LET IR can create closely-spaced, clustered lesions (Chatterjee and Holley, 1991), collisions between low LET particles and atoms in tissues are infrequent, and thus low to moderate levels of low-LET may produce DSBs that are more or less randomly distributed.”
BackgroundSlijepčević, P., & Natarajan, A. T. (1994) · Mutation Research Letters · doi:10.1016/0165-7992(94)90084-1 · Cited by 53
Gamma-H2AX foci in cells exposed to a mixed beam of X-rays and alpha particles
Staaf, E., Brehwens, K., Haghdoost, S., Czub, J., & Wójcik, A. (2012) · Genome Integrity · doi:10.1186/2041-9414-3-8 · Cited by 52 · cited 1×
“(Staaf et al., 2012) reported that gamma (photon) radiation generates as many or more g-H2AX-marked DSB repair foci than doa particles.”
BackgroundWarters, R. L., Newton, G. L., Olive, P. L., & Fahey, R. C. (1999) · Radiation Research · doi:10.2307/3579948 · Cited by 50
Folle, G. A., Martínez‐López, W., Boccardo, E., & Obe, G. (1998) · Mutation research. Fundamental and molecular mechanisms of mutagenesis · doi:10.1016/s0027-5107(98)00090-6 · Cited by 48 · cited 1×
“However, later studies indicated that translocations occur more frequently in euchromatin (reviewed in Folle et al., 1998).”
BackgroundChiu, S., & Oleinick, N. L. (1998) · Radiation Research · doi:10.2307/3579900 · Cited by 48 · cited 1×
“Aswell, small molecules, such as the polyamine spermine, can moderate reactions between ROS and DNA (Spotheim-Maurizot et al., 1995; Chiu and Oleinick, 1998; Warters et al., 1999).”
BackgroundPeriodicity of exonuclease III digestion of chromatin and the pitch of DNA on the nucleosome
Prunell, A. (1983) · Biochemistry · doi:10.1021/bi00290a004 · Cited by 40
Point/Counterpoint: Low-dose radiation is beneficial, not harmful
Doss, M., Little, M. P., & Orton, C. G. (2014) · Medical Physics · doi:10.1118/1.4881095 · Cited by 39 · cited 1×
“There is much less agreement on the risks associated with very low dose IR (e.g., Doss et al., 2014).”
BackgroundSung, W., Park, J. M., Choi, C. H., Ha, S. W., & Ye, S. (2012) · Radiation Oncology Journal · doi:10.3857/roj.2012.30.1.27 · Cited by 36
Radiation-induced Damages in Single- and Double-stranded DNA
Isabelle, V., Prévost, C., Spotheim-Maurizot, M., Sabattier, R., & Charlier, M. (1995) · International Journal of Radiation Biology · doi:10.1080/09553009514550211 · Cited by 36 · cited 1×
“As summarized in Table 2, those atoms are less accessible in DNA with unusually narrow minor grooves (Isabelle et al., 1995).”
BackgroundMaher, R. L., Prasad, A., Rizvanova, O., Wallace, S. S., & Pederson, D. S. (2013) · DNA repair · doi:10.1016/j.dnarep.2013.08.010 · Cited by 34 · cited 2×
“…lesions are repaired varies bothwith the distance between the lesion and the edge of the nucleosome, and the lesion’s helical orientation relative to the underlying histoneoctamer (Odell et al., 2013; also, Menoni et al., 2012; Ye et al., 2012; Maher et al., 2013; Rodriguez and Smerdon, 2013).”
BackgroundSelf-citationComputational biology : new research
Russe, A. S. (2009) · Nova Science Publishers eBooks · Cited by 25
Bunch, R. T., Gewirtz, D. A., & Povirk, L. F. (1995) · International Journal of Radiation Biology · doi:10.1080/09553009514551541 · Cited by 25 · cited 1×
“Aswell, active genes were often found to occur in clusters, surrounded by more radiosensitive chromatin (Bunch et al., 1995).”
BackgroundConsequences and Repair of Oxidative DNA Damage
Duclos, S., Doublié, S., & Wallace, S. S. (2012) · Issues in toxicology · doi:10.1039/9781849732925-00115 · Cited by 22 · cited 1×
“Most such lesions are subject to base excision repair (BER), which entails production of gapped repair intermediates (for reviews, see David et al., 2007; Hegde et al., 2008; Robertson et al., 2009; Duclos et al., 2012; Krokan and Bjoras, 2013; Wallace, 2014).”
BackgroundChromatin Compaction and Tumor Cell Radiosensitivity at 2 Gray
Chapman, J. D., Stobbe, C. C., & Matsumoto, Y. (2001) · American Journal of Clinical Oncology · doi:10.1097/00000421-200110000-00019 · Cited by 14 · cited 1×
“Thus, slow or delayed repair could explain reports of elevated radiation sensitivity in condensed chromatin (Chapman et al., 2001; Stobbeet al., 2002).”
BackgroundNeutron and Gamma-Radiation Sensitivity of Plasmid DNA of Varying Superhelical Density
Swenberg, C. E., & Speicher, J. M. (1995) · Radiation Research · doi:10.2307/3578950 · Cited by 10
Modulation of Enediyne-Induced DNA Damage by Chromatin Structures in Transcriptionally Active Genes
Wu, J., Xu, J. J., & Dedon, P. C. (1999) · Biochemistry · doi:10.1021/bi991999+ · Cited by 8
Research works printed but not linked: 2
- 1998, Strategic program plan for space radiation health research
- 10.1021/bi991999 · DOI
Cited by
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Kay, J. E., Thadhani, E., Samson, L. D., & Engelward, B. P. (2019) · DNA repair · doi:10.1016/j.dnarep.2019.102673 · Cited by 495
Advances in genome editing through control of DNA repair pathways
Yeh, C. D., Richardson, C. D., & Corn, J. E. (2019) · Nature Cell Biology · doi:10.1038/s41556-019-0425-z · Cited by 425
DNA Damage/Repair Management in Cancers
Alhmoud, J. F., Woolley, J. F., Moustafa, A. A., & Malki, M. I. (2020) · Cancers · doi:10.3390/cancers12041050 · Cited by 410
“Genotoxic agents cause structural changes in DNA by disrupting covalent bonds between nucleotides, preventing accurate replication of the genome [3].”
BackgroundBarnes, J. L., Zubair, M., John, K., Poirier, M. C., & Martin, F. L. (2018) · Biochemical Society Transactions · doi:10.1042/bst20180519 · Cited by 320
Karagöz, G. E., Acosta‐Alvear, D., & Walter, P. (2019) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a033886 · Cited by 306
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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