1.中国科学院近代物理研究所 兰州730000
2.中国科学院大学 北京100049
3.兰州理工大学 兰州 730050
4.甘肃省微生物资源开发利用重点实验室 兰州 730070
任军乐,男,1996年9月出生,2021年6月毕业于兰州理工大学,现为中国科学院近代物理研究所生物物理学硕士研究生,E-mail: rjl17393128264@163.com
陆栋,博士生导师,E-mail: ld@impcas.ac.cn
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任军乐, 郭晓鹏, 雷彩荣, 等. 重离子束辐射诱导细胞双链断裂(DSBs)损伤及修复机理的研究进展[J]. 辐射研究与辐射工艺学报, 2023,41(3):030101.
REN Junle, GUO Xiaopeng, LEI Cairong, et al. Progress of research on double-strand break damage induced by heavy-ion beam radiation and repair mechanism[J]. Journal of Radiation Research and Radiation Processing, 2023,41(3):030101.
任军乐, 郭晓鹏, 雷彩荣, 等. 重离子束辐射诱导细胞双链断裂(DSBs)损伤及修复机理的研究进展[J]. 辐射研究与辐射工艺学报, 2023,41(3):030101. DOI: 10.11889/j.1000-3436.2022-0081.
REN Junle, GUO Xiaopeng, LEI Cairong, et al. Progress of research on double-strand break damage induced by heavy-ion beam radiation and repair mechanism[J]. Journal of Radiation Research and Radiation Processing, 2023,41(3):030101. DOI: 10.11889/j.1000-3436.2022-0081.
重离子束辐射能引发细胞DNA双链断裂,被认为是构成基因组不稳定因素之一。现有研究表明:同源末端连接、同源重组、单链退火和选择性末端连接在修复DNA双链断裂方面发挥着重要的作用,但是影响DNA双链断裂修复途径选择的因素目前仍不清楚。本文对近年重离子辐射细胞产生的DNA损伤特征和修复途径方面的新发现进行了综述,并从类型和分布、染色质状态、DNA末端结构、DNA末端切除、细胞周期方面解释了细胞DNA双链断裂修复途径的选择机制。这对细胞DNA损伤修复的研究具有重要意义,为重离子辐射技术在生物学效应研究方面提供了参考。
Heavy-ion beam radiation can cause cell DNA double-strand breaks (DSBs), which are factors that lead to genomic instability. Existing studies have demonstrated that homologous end joining, homologous recombination, single-strand annealing, and selective end joining play critical roles in the repair of DNA DSBs. However, the factors that affect the selection of repair pathways for DNA DSBs remain unclear. In this study, recent findings on DNA damage characteristics and repair pathways generated by heavy-ion radiation cells are reviewed, and the selection mechanism of DSB repair pathways in cells is explained in terms of the types and distribution of DNA DSBs, chromatin status, DNA terminal structures, DNA terminal excision, and cell cycles. This review is of great significance for the study of DNA damage repair and provides a reference for investigating the biological effects of heavy-ion radiation technology.
重离子束辐射DNA损伤簇状DSBsDNA损伤修复
Heavy-ion beam radiationDNA damageClustered DSBsDNA damage repair
缪建顺, 杨建设, 张苗苗, 等. 重离子辐照微生物效应及诱变育种进展[J]. 辐射研究与辐射工艺学报, 2014, 32(2): 3-10.
MIAO Jianshun, YANG Jianshe, ZHANG Miaomiao, et al. Microbial mutagenic effects and mutation breeding advances induced by heavy ion beams[J]. Journal of Radiation Research and Radiation Processing, 2014, 32(2): 3-10.
Durante M, Orecchia R, Loeffler J S. Charged-particle therapy in cancer: clinical uses and future perspectives[J]. NatureReviewsClinicalOncology, 2017, 14(8): 483-495. DOI: 10.1038/nrclinonc.2017.30http://dx.doi.org/10.1038/nrclinonc.2017.30.
Zhang X, Yang F, Ma H Y, et al. Evaluation of the saline-alkaline tolerance of rice (Oryza sativa L.) mutants induced by heavy-ion beam mutagenesis[J]. Biology, 2022, 11(1): 126. DOI: 10.3390/biology11010126http://dx.doi.org/10.3390/biology11010126.
汶瑛, 于雪, 吴玉洁, 等. 重离子诱变微生物育种的研究进展[J]. 微生物学杂志, 2021, 41(6): 66-74. DOI: 10.3969/j.issn.1005-7021.2021.06.009http://dx.doi.org/10.3969/j.issn.1005-7021.2021.06.009.
WEN Ying, YU Xue, WU Yujie, et al. Advanced in microbial breeding by heavy ion mutation[J]. Journal of Microbiology, 2021, 41(6): 66-74. DOI: 10.3969/j.issn.1005-7021.2021.06.009http://dx.doi.org/10.3969/j.issn.1005-7021.2021.06.009.
Ritter S, Durante M. Heavy-ion induced chromosomal aberrations: a review[J]. Mutation Research, 2010, 701(1): 38-46. DOI: 10.1016/j.mrgentox.2010.04.007http://dx.doi.org/10.1016/j.mrgentox.2010.04.007.
Pompos A, Foote R L, Koong A C, et al. National effort to re-establish heavy ion cancer therapy in the United States[J]. Front Oncol, 2022, 12: 880712. DOI: 10.3389/fonc. 2022.880712http://dx.doi.org/10.3389/fonc.2022.880712.
Nikjoo H, O'Neill P, Wilson W E, et al. Computational approach for determining the spectrum of DNA damage induced by ionizing radiation[J]. Radiation Research, 2001, 156(5 Pt 2): 577-583. DOI: 10.1667/0033-7587(2001)156http://dx.doi.org/10.1667/0033-7587(2001)156[0577: cafdts]2.0.co;2.
Friedland W, Schmitt E, Kundrát P, et al. Comprehensive track-structure based evaluation of DNA damage by light ions from radiotherapy-relevant energies down to stopping[J]. ScientificReports, 2017, 7: 45161. DOI: 10. 1038/srep45161http://dx.doi.org/10.1038/srep45161.
Aoki-Nakano M, Furusawa Y. Misrepair of DNA double-strand breaks after exposure to heavy-ion beams causes a peak in the LET-RBE relationship with respect to cell killing in DT40 cells[J]. Journal of Radiation Research, 2013, 54(6): 1029-1035. DOI: 10.1093/jrr/rrt064http://dx.doi.org/10.1093/jrr/rrt064.
Lampe N, Karamitros M, Breton V, et al. Mechanistic DNA damage simulations in Geant4-DNA Part 2: electron and proton damage in a bacterial cell[J]. Physica Medica: PM: an International Journal Devoted to the Applications of Physics to Medicine and Biology: Official Journal of the Italian Association of Biomedical Physics (AIFB), 2018, 48: 146-155. DOI: 10.1016/j.ejmp.2017.12.008http://dx.doi.org/10.1016/j.ejmp.2017.12.008.
Taylor E M, Lehmann A R. Conservation of eukaryotic DNA repair mechanisms[J]. International Journal of Radiation Biology, 1998, 74(3): 277-286. DOI: 10.1080/095530098141429http://dx.doi.org/10.1080/095530098141429.
Hoeijmakers J H J. Genome maintenance mechanisms for preventing cancer[J]. Nature, 2001, 411(6835): 366-374. DOI: 10.1038/35077232http://dx.doi.org/10.1038/35077232.
Santivasi W L, Xia F. Ionizing radiation-induced DNA damage, response, and repair[J]. Antioxidants & Redox Signaling, 2014, 21(2): 251-259. DOI: 10.1089/ars.2013. 5668http://dx.doi.org/10.1089/ars.2013.5668.
Schipler A, Iliakis G. DNA double-strand-break complexity levels and their possible contributions to the probability for error-prone processing and repair pathway choice[J]. Nucleic Acids Research, 2013, 41(16): 7589-7605. DOI: 10.1093/nar/gkt556http://dx.doi.org/10.1093/nar/gkt556.
Mladenov E, Magin S, Soni A, et al. DNA double-strand-break repair in higher eukaryotes and its role in genomic instability and cancer: cell cycle and proliferation-dependent regulation[J]. Seminars in Cancer Biology, 2016, 37/38: 51-64. DOI: 10.1016/j.semcancer.2016. 03.003http://dx.doi.org/10.1016/j.semcancer.2016.03.003.
Burma S, Chen B P C, Chen D J. Role of non-homologous end joining (NHEJ) in maintaining genomic integrity[J]. DNA Repair, 2006, 5(9/10): 1042-1048. DOI: 10.1016/j.dnarep.2006.05.026http://dx.doi.org/10.1016/j.dnarep.2006.05.026.
Iliakis G, Mladenov E, Mladenova V. Necessities in the processing of DNA double strand breaks and their effects on genomic instability and cancer[J]. Cancers, 2019, 11(11): 1671. DOI: 10.3390/cancers11111671http://dx.doi.org/10.3390/cancers11111671.
Scully R, Panday A, Elango R, et al. DNA double-strand break repair-pathway choice in somatic mammalian cells[J]. Nature Reviews Molecular Cell Biology, 2019, 20(11): 698-714. DOI: 10.1038/s41580-019-0152-0http://dx.doi.org/10.1038/s41580-019-0152-0.
Masumura K I, Kuniya K, Kurobe T, et al. Heavy-ion-induced mutations in the gpt delta transgenic mouse: comparison of mutation spectra induced by heavy-ion, X-ray, and gamma-ray radiation[J]. Environmental and Molecular Mutagenesis, 2002, 40(3): 207-215. DOI: 10. 1002/em.10108http://dx.doi.org/10.1002/em.10108.
Yatagai F. Mutations induced by heavy charged particles[J]. Biological Sciences in Space, 2004, 18(4): 224-234. DOI: 10.2187/bss.18.224http://dx.doi.org/10.2187/bss.18.224.
Gollapalle E, Wang R, Adetolu R, et al. Detection of oxidative clustered DNA lesions in X-irradiated mouse skin tissues and human MCF-7 breast cancer cells[J]. Radiation Research, 2007, 167(2): 207-216. DOI: 10. 1667/rr0659.1http://dx.doi.org/10.1667/rr0659.1.
Carter R J, Nickson C M, Thompson J M, et al. Complex DNA damage induced by high linear energy transfer alpha-particles and protons triggers a specific cellular DNA damage response[J]. International Journal of Radiation Oncology*Biology*Physics, 2018, 100(3): 776-784. DOI: 10.1016/j.ijrobp.2017.11.012http://dx.doi.org/10.1016/j.ijrobp.2017.11.012.
Sutherland B M, Bennett P V, Sutherland J C, et al. Clustered DNA damages induced by xrays in human cells[J]. Radiation Research, 2002, 157(6): 611-616. DOI: 10. 1667/0033-7587(2002)157http://dx.doi.org/10.1667/0033-7587(2002)157[0611: cddibx]2.0.co;2.
Asaithamby A, Hu B R, Chen D J. Unrepaired clustered DNA lesions induce chromosome breakage in human cells[J]. Proceedings of the National Academy of Sciences of the United States of America, 2011, 108(20): 8293-8298. DOI: 10.1073/pnas.1016045108http://dx.doi.org/10.1073/pnas.1016045108.
HagiwaraY, OikeT, NiimiA, et al. Clustered DNA double-strand break formation and the repair pathway following heavy-ion irradiation[J]. Journal of Radiation Research, 2019, 60(1): 69-79. DOI: 10.1093/jrr/rry096http://dx.doi.org/10.1093/jrr/rry096.
Soutoglou E, Dorn J F, Sengupta K, et al. Positional stability of single double-strand breaks in mammalian cells[J]. Nature Cell Biology, 2007, 9(6): 675-682. DOI: 10.1038/ncb1591http://dx.doi.org/10.1038/ncb1591.
Desai N, Davis E, O'Neill P, et al. Immunofluorescence detection of clustered gamma-H2AX foci induced by HZE-particle radiation[J]. Radiation Research, 2005, 164(4 Pt 2): 518-522. DOI: 10.1667/rr3431.1http://dx.doi.org/10.1667/rr3431.1.
Nakajima N I, Brunton H, Watanabe R, et al. Visualisation of γH2AX foci caused by heavy ion particle traversal; distinction between core track versus non-track damage[J]. PLoS One, 2013, 8(8): e70107. DOI: 10.1371/journal.pone.0070107http://dx.doi.org/10.1371/journal.pone.0070107.
Oike T, Niimi A, Okonogi N, et al. Visualization of complex DNA double-strand breaks in a tumor treated with carbon ion radiotherapy[J]. Scientific Reports, 2016, 6: 22275. DOI: 10.1038/srep22275http://dx.doi.org/10.1038/srep22275.
Zhao L, Bao C, Shang Y, et al. The determinant of DNA repair pathway choices in ionising radiation-induced DNA double-strand breaks[J]. BioMed Research International, 2020, 2020: 4834965. DOI: 10.1155/2020/4834965http://dx.doi.org/10.1155/2020/4834965.
Lee S E, Moore J K, Holmes A, et al. Saccharomyces Ku70, mre11/rad50 and RPA proteins regulate adaptation to G2/M arrest after DNA damage[J]. Cell, 1998, 94(3): 399-409. DOI: 10.1016/s0092-8674(00)81482-8http://dx.doi.org/10.1016/s0092-8674(00)81482-8.
Matuo Y, Izumi Y, Furusawa Y, et al. Biological effects of carbon ion beams with various LETs on budding yeast Saccharomyces cerevisiae[J]. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 2018, 810: 45-51. DOI: 10.1016/j.mrfmmm.2017.10.003http://dx.doi.org/10.1016/j.mrfmmm.2017.10.003.
Guo X P, Zhang M M, Gao Y, et al. Repair characteristics and time-dependent effects in response to heavy-ion beam irradiation in Saccharomyces cerevisiae: a comparison with X-ray irradiation[J]. Applied Microbiology and Biotechnology, 2020, 104(9): 4043-4057. DOI: 10.1007/s00253-020-10464-8http://dx.doi.org/10.1007/s00253-020-10464-8.
Bhargava R, Onyango D O, Stark J M. Regulation of single-strandannealing and its role in genome maintenance[J]. Trends in Genetics: TIG, 2016, 32(9): 566-575. DOI: 10.1016/j.tig.2016.06.007http://dx.doi.org/10.1016/j.tig.2016.06.007.
Shibata A, Conrad S, Birraux J, et al. Factors determining DNA double-strand break repair pathway choice in G2 phase[J]. The EMBO Journal, 2011, 30(6): 1079-1092. DOI: 10.1038/emboj.2011.27http://dx.doi.org/10.1038/emboj.2011.27.
Yajima H, Fujisawa H, Nakajima N I, et al. The complexity of DNA double strand breaks is a critical factor enhancing end-resection[J]. DNA Repair, 2013, 12(11): 936-946. DOI: 10.1016/j.dnarep.2013.08.009http://dx.doi.org/10.1016/j.dnarep.2013.08.009.
Sridharan D M, Asaithamby A, Bailey S M, et al. Understanding cancer development processes after HZE-particle exposure: roles of ROS, DNA damage repair and inflammation[J]. Radiation Research, 2015, 183(1): 1-26. DOI: 10.1667/RR13804.1http://dx.doi.org/10.1667/RR13804.1.
Shrivastav M, De Haro L P, Nickoloff J A. Regulation of DNA double-strand break repair pathway choice[J]. Cell Research, 2008, 18(1): 134-147. DOI: 10.1038/cr. 2007.111http://dx.doi.org/10.1038/cr.2007.111.
Reindl J, Girst S, Walsh D W M, et al. Chromatin organization revealed by nanostructure of irradiation induced γH2AX, 53BP1 and Rad51 foci[J]. Scientific Reports, 2017, 7: 40616. DOI: 10.1038/srep40616http://dx.doi.org/10.1038/srep40616.
Sridharan D M, Whalen M K, Almendrala D, et al. Increased Artemis levels confer radioresistance to both high and low LET radiation exposures[J]. Radiation Oncology (London, England), 2012, 7: 96. DOI: 10.1186/1748-717X-7-96http://dx.doi.org/10.1186/1748-717X-7-96.
Wang H, Wang X, Zhang P, et al. The Ku-dependent non-homologous end-joining but not other repair pathway is inhibited by high linear energy transfer ionizing radiation[J]. DNA Repair, 2008, 7(5): 725-733. DOI: 10.1016/j.dnarep.2008.01.010http://dx.doi.org/10.1016/j.dnarep.2008.01.010.
Kalousi A, Soutoglou E. Nuclear compartmentalization of DNA repair[J]. Current Opinion in Genetics & Development, 2016, 37: 148-157. DOI: 10.1016/j.gde. 2016.05.013http://dx.doi.org/10.1016/j.gde.2016.05.013.
Krenning L, van den Berg J, Medema R H. Life or death after a break: what determines the choice?[J]. Molecular Cell, 2019, 76(2): 346-358. DOI: 10.1016/j.molcel.2019. 08.023http://dx.doi.org/10.1016/j.molcel.2019.08.023.
Aymard F, Aguirrebengoa M, Guillou E, et al. Genome-wide mapping of long-range contacts unveils clustering of DNA double-strand breaks at damaged active genes[J]. Nature Structural & Molecular Biology, 2017, 24(4): 353-361. DOI: 10.1038/nsmb.3387http://dx.doi.org/10.1038/nsmb.3387.
Lemaître C, Grabarz A, Tsouroula K, et al. Nuclear position dictates DNA repair pathway choice[J]. Genes & Development, 2014, 28(22): 2450-2463. DOI: 10.1101/gad.248369.114http://dx.doi.org/10.1101/gad.248369.114.
Goodarzi A A, Noon A T, Deckbar D, et al. ATM signaling facilitates repair of DNA double-strand breaks associated with heterochromatin[J]. Molecular Cell, 2008, 31(2): 167-177. DOI: 10.1016/j.molcel.2008. 05.017http://dx.doi.org/10.1016/j.molcel.2008.05.017.
Povirk L F, Zhou T, Zhou R Z, et al. Processing of 3'-phosphoglycolate-terminated DNA double strand breaks by Artemis nuclease[J]. Journal of Biological Chemistry, 2007, 282(6): 3547-3558. DOI: 10.1074/jbc.m607745200http://dx.doi.org/10.1074/jbc.m607745200.
Panier S, Boulton S J. Double-strand break repair: 53BP1 comes into focus[J]. Nature Reviews Molecular Cell Biology, 2014, 15(1): 7-18. DOI: 10.1038/nrm3719http://dx.doi.org/10.1038/nrm3719.
Bártová E, Legartová S, Dundr M, et al. A role of the 53BP1 protein in genome protection: structural and functional characteristics of 53BP1-dependent DNA repair[J]. Aging, 2019, 11(8): 2488-2511. DOI: 10.18632/aging.101917http://dx.doi.org/10.18632/aging.101917.
Chapman J R, Sossick A J, Boulton S J, et al. BRCA1-associated exclusion of 53BP1 from DNA damage sites underlies temporal control of DNA repair[J]. Journal of Cell Science, 2012, 125(Pt 15): 3529-3534. DOI: 10.1242/jcs.105353http://dx.doi.org/10.1242/jcs.105353.
Gupta R, Somyajit K, Narita T, et al. DNA repair network analysis reveals shieldin as a key regulator of NHEJ and PARP inhibitor sensitivity[J]. Cell, 2018, 173(4): 972-988.e23. DOI: 10.1016/j.cell.2018.03.050http://dx.doi.org/10.1016/j.cell.2018.03.050.
Schwarz B, Friedl A A, Girst S, et al. Nanoscopic analysis of 53BP1, BRCA1 and Rad51 reveals new insights in temporal progression of DNA-repair and pathway choice[J]. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 2019, 816: 111675. DOI: 10.1016/j.mrfmmm.2019.111675http://dx.doi.org/10.1016/j.mrfmmm.2019.111675.
Averbeck N B, Ringel O, Herrlitz M, et al. DNA end resection is needed for the repair of complex lesions in G1-phase human cells[J]. Cell Cycle (Georgetown, Tex), 2014, 13(16): 2509-2516. DOI: 10.4161/15384101.2015. 941743http://dx.doi.org/10.4161/15384101.2015.941743.
Wu W, Wang M, Wu W,et al. Repair of radiation induced DNA double strand breaks by backup NHEJ is enhanced in G2[J]. DNA Repair, 2008, 7(2): 329-338. DOI: 10. 1016/j.dnarep.2007.11.008http://dx.doi.org/10.1016/j.dnarep.2007.11.008.
Wang M L, Wu W Z, Wu W Q, et al. PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways[J]. Nucleic Acids Research, 2006, 34(21): 6170-6182. DOI: 10.1093/nar/gkl840http://dx.doi.org/10.1093/nar/gkl840.
Hustedt N, Durocher D. The control of DNA repair by the cell cycle[J]. Nature Cell Biology, 2017, 19(1): 1-9. DOI: 10.1038/ncb3452http://dx.doi.org/10.1038/ncb3452.
Aylon Y, Liefshitz B, Kupiec M. The CDK regulates repair of double-strand breaks by homologous recombination during the cell cycle[J]. The EMBO Journal, 2004, 23(24): 4868-4875. DOI: 10.1038/sj.emboj.7600469http://dx.doi.org/10.1038/sj.emboj.7600469.
Huertas P, Cortés-Ledesma F, Sartori A A, et al. CDK targets Sae2 to control DNA-end resection and homologous recombination[J]. Nature, 2008, 455(7213): 689-692. DOI: 10.1038/nature07215http://dx.doi.org/10.1038/nature07215.
Tomimatsu N, Mukherjee B, Catherine Hardebeck M, et al. Phosphorylation of EXO1 by CDKs 1 and 2 regulates DNA end resection and repair pathway choice[J]. Nature Communications, 2014, 5: 3561. DOI: 10.1038/ncomms4561http://dx.doi.org/10.1038/ncomms4561.
Weimer A K, Biedermann S, Schnittger A. Specialization of CDK regulation under DNA damage[J]. Cell Cycle (Georgetown, Tex), 2017, 16(2): 143-144. DOI: 10.1080/15384101.2016.1235852http://dx.doi.org/10.1080/15384101.2016.1235852.
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