Mutagenic consequences of a single G-quadruplex demonstrate mitotic inheritance of DNA replication fork barriers
Open accessAbstract
Faithful DNA replication is vital to prevent disease-causing mutations, chromosomal aberrations and malignant transformation. However, accuracy conflicts with pace and flexibility and cells rely on specialized polymerases and helicases to ensure effective and timely replication of genomes that contain DNA lesions or secondary structures. If and how cells can tolerate a permanent barrier to replication is, however, unknown. Here we show that a single unresolved G-quadruplexed DNA structure can persist through multiple mitotic divisions without changing conformation. Failed replication across a G-quadruplex causes single-strand DNA gaps that give rise to DNA double-strand breaks in subsequent cell divisions, which are processed by polymerase theta (POLQ)-mediated alternative end joining. Lineage tracing experiments further reveal that persistent G-quadruplexes cause genetic heterogeneity during organ development. Our data demonstrate that a single lesion can cause multiple unique genomic rearrangements, and that alternative end joining enables cells to proliferate in the presence of mitotically inherited replication blocks.
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An increased frequency of SNVs can disrupt the normal function and regulation of genes, potentially leading to the development and progression of cancer.
“In this context, we considered local cSNV or dbSNV enrichment as marker for local genomic instability, as an increased frequency of SNVs can disrupt the normal function and regulation of genes, potentially leading to the development and progression of cancer (58).”
From G-quadruplex-mediated genomic instability drives SNVs in cancer (2024) · cites this paper as [58]
The Abstract reports G-quadruplex-induced deletions, and the Discussion compares more extensive rearrangements with those found in cancer cells. Neither passage addresses whether an increased frequency of SNVs disrupts gene function or regulation and contributes to cancer development or progression; searches for SNVs, point mutations, and those cancer effects found no such passage in our copy. (LLM, conf=0.74)
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“What if no homologous donors were available to template repair? A possible insight is provided by analysis of nematodes, where a single quadruplex has been shown to persist through multiple generations, arresting replication to create a 3′ end bordering a gap that is converted to a DSB during DNA replication (27).”
BackgroundCellular Responses to Widespread DNA Replication Stress
Nickoloff, J. A., Jaiswal, A. S., Sharma, N., Williamson, E. A., Tran, M. T., Arris, D., Yang, M., & Hromas, R. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms242316903 · Cited by 43 · see citing works
Pif1 helicase unfolding of G-quadruplex DNA is highly dependent on sequence and reaction conditions
Byrd, A. K., Bell, M. R., & Raney, K. D. (2018) · Journal of Biological Chemistry · doi:10.1074/jbc.ra118.004499 · Cited by 46 · see citing works
“Pif1 has been suggested to resolve G4DNA structures, thereby reducing subsequent formation of DSBs (37) due to unresolved G4DNA persisting through mitosis (38).”
BackgroundHelicase Q promotes homology-driven DNA double-strand break repair and prevents tandem duplications
Kamp, J. A., Lemmens, B., Romeijn, R., Changoer, S. C., van Schendel, R., & Tijsterman, M. (2021) · Nature Communications · doi:10.1038/s41467-021-27408-z · Cited by 35 · see citing works
Self-citationZuo1 supports G4 structure formation and directs repair toward nucleotide excision repair
Magis, A. D., Götz, S., Hajikazemi, M., Fekete-Szücs, E., Caterino, M., Juranek, S., & Paeschke, K. (2020) · Nature Communications · doi:10.1038/s41467-020-17701-8 · Cited by 53 · see citing works
Creation and resolution of non-B-DNA structural impediments during replication
Mellor, C., Perez, C., & Sale, J. E. (2022) · Critical Reviews in Biochemistry and Molecular Biology · doi:10.1080/10409238.2022.2121803 · Cited by 37 · see citing works
“elegans lacking the major G4 helicase DOG-1 (FANCJ), a folded G4 can persist through multiple cell cycles giving rise to a lineage of animals with recurrent deletions at the site of the structure, suggesting that CMG might be able to pass the structure without its resolution (Lemmens et al. 2015).”
Backgroundi-Motif formation and spontaneous deletions in human cells
Martella, M., Pichiorri, F., Chikhale, R., Abdelhamid, M. A. S., Waller, Z. A. E., & Smith, S. S. (2022) · Nucleic Acids Research · doi:10.1093/nar/gkac158 · Cited by 33 · see citing works
“replication completes, either by restarting replication beyond the leading strand impediment or by replication from a distant replication origin two types of structure are created (20,21,36).”
Willis, N. A., Panday, A., Duffey, E. E., & Scully, R. (2018) · PLoS Genetics · doi:10.1371/journal.pgen.1007486 · Cited by 29 · see citing works
Unravelling roles of error-prone DNA polymerases in shaping cancer genomes
Vaziri, C., Rogozin, I. B., Gu, Q., Wu, D., & Day, T. A. (2021) · Oncogene · doi:10.1038/s41388-021-02032-9 · Cited by 32 · see citing works
“Notably, the boundaries of these polq-dependent deletions occurred overwhelmingly at the edge of G4 DNA structures [70, 71].”
BackgroundSpotlight on G-Quadruplexes: From Structure and Modulation to Physiological and Pathological Roles
dell’Oca, M. C., Quadri, R., Bernini, G. M., Menin, L., Grasso, L., Rondelli, D., Yazici, O., Sertic, S., Marini, F., Pellicioli, A., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25063162 · Cited by 29 · see citing works
“However, when these factors are depleted or inactive, the G-quadruplex becomes an obstacle to replicative fork progression, leaving an exposed ssDNA stretch that eventually generates a double-strand break [286,287].”
BackgroundDuskova, K., Lamarche, J., Amor, S., Caron, C., Queyriaux, N., Gaschard, M., Penouilh, M., Robillard, G., Delmas, D., Devillers, C. H., et al. (2019) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.8b01978 · Cited by 36 · see citing works
DNA Ligase 1 is an essential mediator of sister chromatid telomere fusions in G2 cell cycle phase
Liddiard, K., Ruis, B. L., Kan, Y., Cleal, K., Ashelford, K. E., Hendrickson, E. A., & Baird, D. M. (2018) · Nucleic Acids Research · doi:10.1093/nar/gky1279 · Cited by 28 · see citing works
“LIG1 complexed with PCNA and unligated Okazaki fragments may nucleate fusion of leading and lagging strand DNA, facilitated by POLQ helicase activity (82,104) and stabilized by POLQ-mediated DNA synthesis (63,105).”
Richardson, T. E., Walker, J. M., Hambardzumyan, D., Brem, S. S., Hatanpaa, K. J., Viapiano, M. S., Pai, B., Umphlett, M., Becher, O. J., Snuderl, M., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02761-7 · Cited by 28 · see citing works
“…the availability of nucleotides, DNA damage, and formation of secondary DNA structures (such as guanine-rich quadruplexes, which may be crucial to genetic instability with ATRX inactivation) [54, 115, 119, 164, 184, 202, 221], which pause replication and histone recycling/incorporation [96, 97].”
BackgroundBournique, E., Dall’Osto, M., Hoffmann, J., & Bergoglio, V. (2017) · Mutation research. Fundamental and molecular mechanisms of mutagenesis · doi:10.1016/j.mrfmmm.2017.08.002 · Cited by 23 · see citing works
DNA G-Quadruplexes as Targets for Natural Product Drug Discovery
Wang, K.-B., Wang, Y., Dickerhoff, J., & Yang, D.-Z. (2024) · Engineering · doi:10.1016/j.eng.2024.03.015 · Cited by 24 · see citing works
“In addition, G4 formation can cause site mutagenesis, gene deletion–junction, transposition, rearrangement, and copy number alterations, which are important sources of genome instability and disease genesis [174,175].”
Variation in G-quadruplex sequence and topology differentially impacts human DNA polymerase fidelity
Stein, M., Hile, S. E., Weissensteiner, M. H., Lee, M., Zhang, S., Kejnovský, E., Kejnovská, I., Makova, K. D., & Eckert, K. A. (2022) · DNA Repair · doi:10.1016/j.dnarep.2022.103402 · Cited by 23 · see citing works
Lee, W. T. C., Yin, Y., Morten, M. J., Tonzi, P., Gwo, P. P., Odermatt, D. C., Modesti, M., Cantor, S. B., Gari, K., Huang, T. T., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-22830-9 · Cited by 107 · see citing works
Getting Ready for the Dance: FANCJ Irons Out DNA Wrinkles
Bharti, S., Awate, S., Banerjee, T., & Brosh, R. M. (2016) · Genes · doi:10.3390/genes7070031 · Cited by 22 · see citing works
“Evidence from worm studies suggest that a single G4 causes a persistent replication block that elicits the alternative end‐joining pathway resulting in multiple genomic deletions at one genomic location; however, the frequency of characteristic small‐sized deletions near the G4 motif were not exacerbated in dog‐1 muta…”
BackgroundG-quadruplex-mediated genomic instability drives SNVs in cancer
Richl, T., Kuper, J., & Kisker, C. (2024) · Nucleic Acids Research · doi:10.1093/nar/gkae098 · Cited by 20 · see citing works
“In this context, we considered lo-cal cSNV or dbSNV enrichment as marker for local genomic instability, as an increased frequency of SNVs can disrupt the normal function and regulation of genes, potentially leading to the development and progression of cancer ( 58 ).”
BackgroundIdentification of G-quadruplex forming sequences in three manatee papillomaviruses
Zahin, M., Dean, W., Ghim, S., Joh, J., Gray, R., Khanal, S., Bossart, G., Mignucci-Giannoni, A., Rouchka, E., Jenson, A., et al. (2018) · PLoS ONE · doi:10.1371/journal.pone.0195625 · Cited by 20 · see citing works
“The G4 secondary structures are known to be mutagenic [61] , and in HIV-1 and HIV-2, mutated capsids are known to affect the ability of dendritic cells to detect the virus [62] .”
van Schendel, R., Romeijn, R., Buijs, H., & Tijsterman, M. (2021) · Science Advances · doi:10.1126/sciadv.abf2278 · Cited by 19 · see citing works
Self-citationFundamentals of G-quadruplex biology
Johnson, F. B. (2020) · Annual reports in medicinal chemistry · doi:10.1016/bs.armc.2020.06.004 · Cited by 27 · see citing works
“as a chromatid with a single stranded gap), and when the incompletely replicated strand is itself used as a replication template in the next cell cycle, this leads to double strand DNA breaks that are repaired by DNA polymerase theta-dependent end-joining to generate the deletion.(133,134) Similarly, human cells lacki…”
Stein, M., & Eckert, K. A. (2021) · Genes · doi:10.3390/genes12111779 · Cited by 20 · see citing works
“Deletions were primarily observed at the 3′ flanking sequence of a G4, which indirectly suggested to the authors the occurrence of polymerase stalling [41,42].”
BackgroundG-quadruplex in animal development: Contribution to gene expression and genomic heterogeneity
Armas, P., & Calcaterra, N. B. (2018) · Mechanisms of Development · doi:10.1016/j.mod.2018.05.004 · Cited by 19 · see citing works
Wang, S., Lu, S., Zhao, J., Huang, J.-S., & Yang, X.-R. (2017) · ACS Applied Materials and Interfaces · doi:10.1021/acsami.7b13477 · Cited by 18
Structural Motifs at the Telomeres and Their Role in Regulatory Pathways
Alanazi, A. F. R., Parkinson, G. N., & Haider, S. (2024) · Biochemistry · doi:10.1021/acs.biochem.4c00023 · Cited by 18
“123 In the absence of Pif1, these sites are susceptible to double breaks.”
Polymerase θ Coordinates Multiple Intrinsic Enzymatic Activities during DNA Repair
Zahn, K., & Jensen, R. B. (2021) · Genes · doi:10.3390/genes12091310 · Cited by 17
“Theta-mediated end-joining (TMEJ) [21] accounts for a major portion of the MMEJ signatures arising as genetic scars of DSB repair (Figure 1b).”
BackgroundSweet Melody or Jazz? Transcription Around DNA Double-Strand Breaks
Long, Q., Liu, Z., & Gullerová, M. (2021) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2021.655786 · Cited by 17 · see citing works
J, V. K. M., Mitteaux, J., Wang, Z., Wheeler, E., Tandon, N., Jung, S. Y., Hudson, R. H. E., Monchaud, D., & Tsvetkov, A. S. (2024) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2024.108040 · Cited by 17 · see citing works
Кузнецова, А. А., Fedorova, O. S., & Kuznetsov, N. A. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.595687 · Cited by 17 · see citing works
A Novel G-Quadruplex Binding Protein in Yeast—Slx9
Götz, S., Pandey, S., Bartsch, S., Juranek, S., & Paeschke, K. (2019) · Molecules · doi:10.3390/molecules24091774 · Cited by 18 · see citing works
G-quadruplex structure at intron 2 of TFE3 and its role in Xp11.2 translocation and splicing.
Verma, S. P., & Das, P. (2018) · Biochimica et Biophysica Acta - General Subjects · doi:10.1016/j.bbagen.2017.11.011 · Cited by 15 · see citing works
Lorenzatti, A., Piga, E. J., Gismondi, M., Binolfi, A., Margarit, E., Calcaterra, N., & Armas, P. (2022) · bioRxiv · doi:10.1093/nar/gkad948 · Cited by 14 · see citing works
“G4s, along with other non-B DNA structures, have emerged as major contributors to genome-wide SNVs by disrupting replication and transcription ( 65–68 ), thus leading to genetic diversity ( 29–32 , 69 , 70 ) and probably causing at least part of the G4-Vars.”
BackgroundStructural mechanism underpinning Thermus oshimai Pif1‐mediated G‐quadruplex unfolding
Dai, Y., Guo, H.-L., Liu, N.-N., Chen, W.-F., Ai, X., Li, H.-H., Sun, B., Hou, X.-M., Réty, S., & Xi, X.-G. (2022) · EMBO Reports · doi:10.15252/embr.202153874 · Cited by 14 · see citing works
“…with G 4 To probe the structural basis of To Pif1-mediated G4 unfolding, To Pif1 was complexed with parallel and antiparallel G4 DNAs flanked at their 5 0 - and 3 0 - ends with 6 and 8 nt poly(dT), respectively, mimicking G4s formed at a replication fork (Lemmens et al , 2015; Lee et al , 2021).”
TWJ-Screen: an isothermal screening assay to assess ligand/DNA junction interactions in vitro
Guyon, L., Pirrotta, M., Duskova, K., Granzhan, A., Teulade‐Fichou, M., & Monchaud, D. (2017) · Nucleic Acids Research · doi:10.1093/nar/gkx1118 · Cited by 21 · see citing works
Wanzek, K., Schwindt, E., Capra, J. A., & Paeschke, K. (2017) · Nucleic Acids Research · doi:10.1093/nar/gkx467 · Cited by 17 · see citing works
Suseela, Y. V., Sengupta, P., Roychowdhury, T., Panda, S., Talukdar, S., Chattopadhyay, S., Chatterjee, S., & Govindaraju, T. (2021) · ACS Bio & Med Chem Au · doi:10.1021/acsbiomedchemau.1c00039 · Cited by 12 · see citing works
Mgs1 function at G-quadruplex structures during DNA replication
Paeschke, K., & Burkovics, P. (2020) · Current Genetics · doi:10.1007/s00294-020-01128-1 · Cited by 11 · see citing works
Amparo, C., Clark, J. P., Bedell, V., Murata-Collins, J., Martella, M., Pichiorri, F., Warner, E., Abdelhamid, M. A. S., Waller, Z. A. E., & Smith, S. S. (2020) · Cancer Genomics & Proteomics · doi:10.21873/cgp.20171 · Cited by 12 · see citing works
Plant-GQ: An Integrative Database of G-Quadruplex in Plant
Ge, F., Wang, Y., Li, H., Zhang, R., Wang, X., Li, Q., Liang, Z.-C., & Yang, L. (2019) · J. Comput. Biol. · doi:10.1089/cmb.2019.0010 · Cited by 11
“…(Moye et al., 2015; Noer et al., 2016), promoters (Beaume et al., 2013; Voter et al., 2018), mitotic and meiotic double-strand break sites (Lemmens et al., 2015), ribosomal DNA (Wallgren et al., 2016), transcriptional start sites (Morgan et al., 2016), and untranslated regions of…”
Combined loss of three DNA damage response pathways renders C. elegans intolerant to light
van Bostelen, I., & Tijsterman, M. (2017) · DNA repair · doi:10.1016/j.dnarep.2017.04.002 · Cited by 11 · see citing works
“For a discussion on why replication-associated DSBs at persistent lesions are exclusive substrates for TMEJ and not for classical NHEJ or HR we wish to refer the reader to recently published work that addresses this issue using G-quadruplexes as a model substrate to block DNA replication [53,54].”
BackgroundSelf-citationAnalysis of mutational signatures in C. elegans: Implications for cancer genome analysis
Meier, B., Volkova, N. V., Gerstung, M., & Gartner, A. (2020) · DNA repair · doi:10.1016/j.dnarep.2020.102957 · Cited by 16 · see citing works
Sequence Dynamics of Pre-mRNA G-Quadruplexes in Plants
Kopec, P. M., & Karłowski, W. (2019) · Frontiers in Plant Science · doi:10.3389/fpls.2019.00812 · Cited by 9
How DNA secondary structures drive replication fork instability
Sethi, A., Fernández-Casañas, M., Delpino, B., & Coster, G. (2025) · DNA repair · doi:10.1016/j.dnarep.2025.103913 · Cited by 7 · see citing works
Werner helicase interacting protein 1 contributes to G-quadruplex processing in human cells
Hegedűs, L., Toth, A., Harami, G. M., Pálinkás, J., Karatayeva, N., Sajben-Nagy, E., Bene, S., Jaktajdinani, S. A., Kovács, M., Juhász, S., et al. (2024) · Scientific Reports · doi:10.1038/s41598-024-66425-y · Cited by 7 · see citing works
“Stable secondary structures forming on single stranded nucleic acids, such as G4 quadruplexes, can induce replication fork pausing which can lead to the formation of DNA lesions, including DSBs.”
BackgroundSengupta, P., Dutta, A., Suseela, Y. V., Roychowdhury, T., Banerjee, N., Dutta, A., Halder, S., Jana, K., Mukherjee, G., Chattopadhyay, S., et al. (2024) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-023-05046-6 · Cited by 7
“…analyses have further suggested that G4 structures are concentrated within the functional genomic regions, from highly divergent organisms, and play imperative roles in myriad gene-regulatory functions, such as transcription, replication, telomere maintenance, and translation regulation [34–37].”
G-quadruplexes in Prague: A Bohemian Rhapsody.
O'Hagan, M. P., Mergny, J., & Waller, Z. A. E. (2018) · Biochimie · doi:10.1016/j.biochi.2018.02.004 · Cited by 7 · see citing works
G-quadruplex stabilization via small molecules as a potential anti-cancer strategy
Li, C., Liu, J., & Wang, R. (2026) · Cellular & Molecular Biology Letters · doi:10.1186/s11658-026-00890-3 · Cited by 6 · see citing works
“4) [105].”
Computer Folding of Parallel DNA G‐Quadruplex: Hitchhiker's Guide to the Conformational Space
Janeček, M., Kührová, P., Mlýnský, V., Stadlbauer, P., Otyepka, M., Bussi, G., Šponer, J., & Banáš, P. (2024) · Journal of Computational Chemistry · doi:10.1002/jcc.27535 · Cited by 7 · see citing works
Hron, T., Miklík, D., Pačes, J., Pajer, P., Pečenka, V., Hejnar, J., Nehyba, J., & Elleder, D. (2025) · bioRxiv · doi:10.1093/gbe/evag038 · Cited by 5 · see citing works
“One possibility is the involvement of mitotic and DNA repair processes, which might be reinforced in genomic loci under replication stress caused by high GC content or DNA secondary structures (Kruisselbrink et al. 2008; Lemmens et al. 2015; Kamp et al. 2021).”
Bulged and Canonical G-Quadruplex Conformations Determine NDPK Binding Specificity
Kopylov, M., Jackson, T. M., & Stroupe, M. E. (2019) · Molecules · doi:10.3390/molecules24101988 · Cited by 5
Zhang, M., Liu, R., & Wang, F. (2019) · Methods in molecular biology · doi:10.1007/978-1-4939-9500-4_23 · Cited by 5 · see citing works
ssG4-seq for global profiling of strand-specific G-quadruplex structures in mammalian genomes
Li, S., Wang, R., Zhang, J., Cao, C., Bai, J., Cai, Z., Ye, R., Chen, J., Liu, W., Chen, L., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-66895-2 · Cited by 5 · see citing works
Towards 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 · see citing works
Brahme, A. (2022) · Radiation Research · doi:10.1667/rade-22-00011.1 · Cited by 4 · see citing works
“Beside the many non-homologous and homology directed repair (HDR) systems discussed there, one should add the polymerase h based TMEJ [analogous to MHEJ but largely independent of PARP 1 (43, 44); cf.”
BackgroundSpontaneous DNA Synapsis by Forming Noncanonical Intermolecular Structures
Severov, V. V. V., Tsvetkov, V., Barinov, N., Babenko, V., Klinov, D. D. V., & Pozmogova, G. G. E. (2021) · bioRxiv · doi:10.3390/polym14102118 · Cited by 4 · see citing works
Distinct sequence features underlie microdeletions and gross deletions in the human genome
Qi, M., Stenson, P., Ball, E. V., Tainer, J., Bacolla, A., Kehrer-Sawatzki, H., Cooper, D., & Zhao, H.-Y. (2021) · Human Mutation · doi:10.1002/humu.24314 · Cited by 4 · see citing works
“B DNA structures often have key regulatory functions in DNA replication and transcription but may also cause genomic instability (Lemmens et al., 2015; Zhao et al., 2010).”
BackgroundA mutational scar-based genome-wide map of DNA double-strand break repair
Barazas, M., van Schendel, R., & Tijsterman, M. (2026) · Nature Communications · doi:10.1038/s41467-026-72744-7 · Cited by 8 · see citing works
“Consistent with this feature pointing to underlying TMEJ activity 12 – 14 , expression of the HRD signature is dependent on POLQ 15 , and HRD tumour cells exhibit a pronounced reliance on POLQ for survival 16,17 .”
Self-citationPolymerase theta: Genome protection through regulated deployment.
Smith, C. M., & Gupta, G. P. (2025) · DNA Repair · doi:10.1016/j.dnarep.2025.103916 · Cited by 3
- Authors
- Lemmens, B., van Schendel, R., & Tijsterman, M.
- Affiliations
- Leiden University Medical Center (NL)
- Corresponding author
- Tijsterman, Marcel
- Venue
- Nature Communications
- Published
- 2015-11-13
- Volume
- 6
- Issue
- 1
- Pages
- 8909-8909
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4654259
- OpenAlex
- W2296534952
- Cited by
- 133
- References
- 30
- Citations by year
- 2026: 10 · 2025: 10 · 2024: 13 · 2023: 9 · 2022: 8 · 2021: 19 · 2020: 16 · 2019: 18 · 2018: 10 · 2017: 12 · 2016: 8
- FWCI
- 4.34
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Leiden Repository (Leiden University) (submittedVersion)
- Funders
- European Commission
- ZonMw
- National Institutes of Health (OD010440, P40OD010440)
- FP7 Ideas: European Research Council (203379)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- G-quadruplex, mitotic inheritance, mutagenesis, DNA double-strand breaks, alternative end-joining, polymerase theta, genome rearrangement, lineage tracing, DNA secondary structure, DNA damage tolerance
- MeSH terms
- Animals, DNA Replication, Mitosis, Mutagenesis, Caenorhabditis elegans, Cell Proliferation, DNA Breaks, Double-Stranded, G-Quadruplexes
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