Cited by 313DNA Repair MechanismsEffects of Radiation ExposurePARP inhibition in cancer therapy

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The controlling role of ATM in homologous recombinational repair of DNA damage

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Morrison, Ciaran, Sonoda, Eiichiro, Takao, Noriaki, Shinohara, Akira, Yamamoto, Ken‐ichi, Takeda, Shunichi·2000·The EMBO Journal

DOI 10.1093/emboj/19.3.463PMC PMC305583

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Abstract

The human genetic disorder ataxia telangiectasia (A-T), caused by mutation in the ATM gene, is characterized by chromosomal instability, radiosensitivity and defective cell cycle checkpoint activation. DNA double-strand breaks (dsbs) persist in A-T cells after irradiation, but the underlying defect is unclear. To investigate ATM's interactions with dsb repair pathways, we disrupted ATM along with other genes involved in the principal, complementary dsb repair pathways of homologous recombination (HR) or non-homologous end-joining (NHEJ) in chicken DT40 cells. ATM(-/-) cells show altered kinetics of radiation-induced Rad51 and Rad54 focus formation. Ku70-deficient (NHEJ(-)) ATM(-/-) chicken DT40 cells show radiosensitivity and high radiation-induced chromosomal aberration frequencies, while Rad54-defective (HR(-)) ATM(-/-) cells show only slightly elevated aberration levels after irradiation, placing ATM and HR on the same pathway. These results reveal that ATM defects impair HR-mediated dsb repair and may link cell cycle checkpoints to HR activation.

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Method
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BackgroundSelf-citation
ATM-dependent activation of SIM2s regulates homologous recombination and epithelial–mesenchymal transition
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Background
DNA-Dependent Protein Kinase and Ataxia Telangiectasia Mutated (ATM) Promote Cell Survival in Response to NK314, a Topoisomerase IIα Inhibitor
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Background
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Self-citation
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Background
Methylation of TMEM176A , a key ERK Signaling Regulator, is a Novel Synthetic Lethality Marker of ATM Inhibitors in Human Lung Cancer
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ATM modulates subventricular zone neural stem cell maintenance and senescence through Notch signaling pathway
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Persistence of unrepaired DNA double strand breaks caused by inhibition of ATM does not lead to radio-sensitisation in the absence of NF-κB activation
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Sampath, D., & Plunkett, W. K. (2007) · Current Oncology Reports · doi:10.1007/s11912-007-0048-6 · Cited by 15
“This process requires the function of the ataxia telangiectasia mutated protein (ATM) kinase, which is a member of the PI3-K family of protein kinases that also includes DNA-PK [ 19 ].”
Background
Niraparib as Maintenance Therapy in Germline ATM-mutated and Somatic BRCA2-mutated Ovarian Cancer with Brain Metastases: A Case Report and Literature Review
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The involvement of WT1 in the regulation of GADD45a in response to genotoxic stress
Johnson, D., Hastwell, P. W., & Walmsley, R. M. (2013) · Mutagenesis · doi:10.1093/mutage/get015 · Cited by 14
“Double-strand breaks resulting from MMS exposure are likely to trigger this response pathway as ATM is involved in both homologous recombination and nonhomologous end joining DSB repair pathways (16,28).”
Background
ATM depletion induces proteasomal degradation of FANCD2 and sensitizes neuroblastoma cells to PARP inhibitors
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Takeishi, Y., Iwaya-Omi, R., Ohashi, E., & Tsurimoto, T. (2015) · Journal of Biological Chemistry · doi:10.1074/jbc.m115.669002 · Cited by 13
“In human cells, ATM mainly reacts to double strand breaks (DSBs) (7, 8) and activates nonhomologous end-joining or homologous recombination (HR) (9, 10).”
Background
Selective tumor killing based on specific DNA-damage response deficiencies
Biss, M., & Xiao, W. (2012) · Cancer Biology & Therapy · doi:10.4161/cbt.18921 · Cited by 13
The rate of extrachromosomal homologous recombination within a novel reporter plasmid is elevated in cells lacking functional ATM protein
Drexler, G. A., Wilde, S., Beisker, W., Ellwart, J. W., Eckardt‐Schupp, F., & Fritz, E. (2004) · DNA repair · doi:10.1016/j.dnarep.2004.05.001 · Cited by 13
REV3 promotes cellular tolerance to 5-fluorodeoxyuridine by activating translesion DNA synthesis and intra-S checkpoint
Washif, M., Kawasumi, R., & Hirota, K. (2024) · PLoS Genetics · doi:10.1371/journal.pgen.1011341 · Cited by 12
Tumor suppressor RecQL5 controls recombination induced by DNA crosslinking agents
Hosono, Y., Abe, T., Ishiai, M., Islam, M. N., Arakawa, H., Wang, W., Takeda, S., Ishii, Y., Takata, M., Seki, M., et al. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2014.01.005 · Cited by 12
“For this purpose, we generated RECQL5/RAD54 double KO cells using conditional RAD54 KO cells (RAD54−/− + hRAD54-HA cells) as the parental cell line [37], in which expression of human RAD54-HA protein is suppressed by doxycyclin (Dox) treatment, because of the possibility of synthetic lethality (Fig.”
MethodSelf-citation
RAD52 Adjusts Repair of Single-Strand Breaks via Reducing DNA-Damage-Promoted XRCC1/LIG3α Co-localization
Wang, J., Oh, Y.-T., Li, Z., Dou, J., Tang, S., Wang, X., Wang, H., Takeda, S., & Wang, Y. (2021) · Cell Reports · doi:10.1016/j.celrep.2020.108625 · Cited by 12
Self-citation
UV Irradiation Causes the Loss of Viable Mitotic Recombinants in Schizosaccharomyces pombe Cells Lacking the G2/M DNA Damage Checkpoint
Osman, F., Tsaneva, I. R., Whitby, M. C., & Doe, C. L. (2002) · Genetics · doi:10.1093/genetics/160.3.891 · Cited by 12
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The role of human replicative DNA polymerases in DNA repair and replication
Rytkönen, A. K. (2006) · Cited by 11
TOWARD MAINTAINING THE GENOME
Nyberg, K. A., Michelson, R. J., Putnam, C. W., & Weinert, T. A. (2002) · Cited by 10
Proofreading exonuclease activity of replicative polymerase epsilon promotes cellular tolerance to arabinosides in CTF18-dependent and -independent manner
Rahman, M. R., Hirota, K., & Kawasumi, R. (2024) · Genome Instability & Disease · doi:10.1007/s42764-024-00124-w · Cited by 9
“…removal of nucleoside analogs ( POLE1 exo−/− , CTF18 −/− ) (Tsuda et al., 2017; Washif et al., 2023), checkpoint control ( ATM −/− , RAD17 /− ) (Morrison et al., 2000; Saberi et al., 2008), and sister chromatid cohesion ( DDX11 −/− , SA2 −/− ) (Abe et al., 2016; Kawasumi et al., 2021) (Table…”
RAD18 ‐ and BRCA1 ‐dependent pathways promote cellular tolerance to the nucleoside analog ganciclovir
Ahmad, T., Kawasumi, R., & Hirota, K. (2024) · Genes to Cells · doi:10.1111/gtc.13155 · Cited by 9
Analysis of the relationships between ATM and the Rad54 paralogs involved in homologous recombination repair
Kirshner, M., Rathavs, M., Nizan, A., Essers, J., Kanaar, R., Shiloh, Y., & Barzilai, A. (2008) · DNA repair · doi:10.1016/j.dnarep.2008.11.005 · Cited by 9
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Osterman, M. D., Kathawa, D., Liu, D., Guo, H., Zhang, C., Li, M., Yu, X., & Li, F. (2014) · Histochemistry and Cell Biology · doi:10.1007/s00418-014-1245-7 · Cited by 10
“2012), which further links DNA damages to pancreatic cancers since ATM is a core kinase in DNA damage response network and impairment of ATM could result in the failure of DNA repair (Matsuoka et al. 2007; Morrison et al. 2000).”
Background
Heavy water inhibits DNA double-strand break repairs and disturbs cellular transcription, presumably via quantum-level mechanisms of kinetic isotope effects on hydrolytic enzyme reactions
Yasuda, T., Nakajima, N. I., Ogi, T., Yanaka, T., Tanaka, I., Gotoh, T., Kagawa, W., Sugasawa, K., & Tajima, K. (2024) · PLoS ONE · doi:10.1371/journal.pone.0309689 · Cited by 9
Cytotoxic and genotoxic effects of dioxacarb by human peripheral blood lymphocytes CAs and Allium test
Eren, Y., Erdoğmuş, S. F., Akyıl, D., Özkara, A., Konuk, M., & Sağlam, E. (2014) · Cytotechnology · doi:10.1007/s10616-014-9741-0 · Cited by 8
“Clastogenic agents may induce DNA double-strand breaks and lead to either cell cycle arrest or apoptosis (Kastan et al. 1991; Bunz et al. 1998; Morrison et al. 2000; Obe and Durante 2010).”
Background
Caffeine-inhibitable control of the radiation-induced G2 arrest in L5178Y-S cells deficient in non-homologous end-joining
Szumiel, I., Kapiszewska, M., John, A., Grądzka, I., Kowalczyk, D. W., & Janik, P. (2001) · Radiation and Environmental Biophysics · doi:10.1007/s004110100089 · Cited by 8
“Atm controls the activity of recombination repair [ 40 ], which in LY-S cells appears to be the main one that is functioning upon x-irradiation [18, 24].”
Background
Therapeutic Targeting of DNA Repair Pathways in Pediatric Extracranial Solid Tumors: Current State and Implications for Immunotherapy
Zhao, S. J., Prior, D., Heske, C. M., & Vasquez, J. C. (2024) · Cancers · doi:10.3390/cancers16091648 · Cited by 7
“The Ataxia telangiectasia mutated gene ( ATM ) encodes a serine-threonine protein kinase that is a main transducer of target proteins involved in the DNA DSB repair pathways NHEJ and HRR [23,24].”
Background
Drugging the DNA damage response in the clinic: going beyond PARP
Torrado, C., González-Ortiz, Á., Xavier, C. B., Tan, H. N., Ngoi, N. Y. L., & Yap, T. A. (2025) · Expert Review of Anticancer Therapy · doi:10.1080/14737140.2025.2575825 · Cited by 8
“Although ATM deficiency impairs DSB repair and causes radiosensitivity, ATM is dispensable for HRR in some contexts, as ATM -deficient cells are less sensitive to cross-linking agents than HR -deficient cells [97–101].”
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Hosen, M. B., Kawasumi, R., & Hirota, K. (2024) · DNA repair · doi:10.1016/j.dnarep.2024.103668 · Cited by 7
PrimPol-mediated repriming elicits gap-filling by template switching and promotes cellular tolerance to cidofovir
Washif, M., Kawasumi, R., & Hirota, K. (2024) · DNA repair · doi:10.1016/j.dnarep.2024.103787 · Cited by 7
Twilight effects of low doses of ionizing radiation on cellular systems: a bird’s eye view on current concepts and research
Postiglione, I., Chiaviello, A., & Palumbo, G. A. (2009) · Medical Oncology · doi:10.1007/s12032-009-9241-9 · Cited by 7
“In addition, ATM deficiency results in severe meiotic disruption [74, 75].”
Background
Flavopiridol: where do we stand in chronic lymphocytic leukemia?
Lin, T. S., & Porcu, P. (2003) · Leukemia · doi:10.1038/sj.leu.2403237 · Cited by 7
The flap endonuclease-1 mediated maturation of Okazaki fragments is critical for the cellular tolerance to remdesivir
Rahman, M. R., Kawasumi, R., & Hirota, K. (2024) · DNA repair · doi:10.1016/j.dnarep.2024.103773 · Cited by 6
Disruption of the BLM gene in ATM-null DT40 cells does not exacerbate either phenotype
Fukao, T., Chen, P., Ren, J., Kaneko, H., Zhang, G. X., Kondo, M., Yamamoto, K.-I., Furuichi, Y., Takeda, S., Kondo, N., et al. (2004) · Oncogene · doi:10.1038/sj.onc.1207276 · Cited by 6
“More direct evidence for such a role has been provided by disrupting ATM in combination with genes involved in the major repair pathways for DNA double-strand break rejoining (Morrison et al., 2000).”
BackgroundSelf-citation
Ataxia telangiectasia mutated (ATM) kinase as a predictive biomarker in clinical oncology: implications for a precision treatment approach
Pham, A. T., Yuan, F., Nagathihalli, N. S., & Dosch, A. R. (2026) · Neoplasia · doi:10.1016/j.neo.2026.101309 · Cited by 5
“Numerous additional studies have implicated ATM as a key mediator of HR repair mechanisms, although it is not considered a core HR protein[66 – 68].”
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Wang, W., Seki, M., Otsuki, M., Tada, S., Takao, N., Yamamoto, K.-I., Hayashi, M., Honma, M., & Enomoto, T. (2003) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2003.11.008 · Cited by 5
“It has been reported that a defect of ATM causes the slower accumulation of RAD51 foci in response to ionizing radiation [31], and ATM phosphorylates BRCA1, NBS1 and Rad51 [32–35].”
BackgroundSelf-citation
Coordinate to Guard: Crosstalk of Phosphorylation, Sumoylation, and Ubiquitylation in DNA Damage Response
Kuo, C., Shieh, C., Cai, F., & Ann, D. K. (2012) · Frontiers in Oncology · doi:10.3389/fonc.2011.00061 · Cited by 5
“A-T cells do not exhibit cell cycle arrest at regular checkpoints when stressed by irradiation (Morrison et al., 2000).”
Background
Genomic Instability:Signaling Pathways Orchestrating the Responsesto Ionizing Radiation and Cisplatin
Sakamoto‐Hojo, E. T., Mello, S. S., Bassi, C. L., Merchi, I. M., Carminati, P. O., Fachin, A. L., Donadi, E. A., & Passos, G. A. S. (2005) · Genome dynamics and stability · doi:10.1007/7050_010 · Cited by 4
“Studies in DT40 cells demonstrated that ATM deficiency impairs HR-mediated DSB repair and that this protein may link the cell-cycle checkpoints to HR activation (Morrison et al. 2000; Yuan et al. 2003).”
Background
Cancer Cells Haploinsufficient for ATM Are Sensitized to PARP Inhibitors by MET Inhibition
D’Ambrosio, C., Erriquez, J., Capellero, S., Cignetto, S., Alvaro, M., Ciamporcero, E. S., Renzo, M. F. D., Perera, T. P. S., Valabrega, G., & Olivero, M. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23105770 · Cited by 4
“Among the latter, ataxia telangiectasia mutated (ATM) is a DNA damage checkpoint also able to indirectly activate homologous recombination repair [7] and/or to counter toxic non-homologous end-joining (NHEJ) at broken replication forks [8].”
Background
TEL1 from Saccharomyces cerevisiae suppresses chromosome aberrations induced by ionizing radiation in ataxia-telangiectasia cells without affecting cell cycle checkpoints
Cao, J.-P., Meyn, M. S., Eckardt‐Schupp, F., & Fritz, E. (2001) · Radiation and Environmental Biophysics · doi:10.1007/s00411-001-0125-4 · Cited by 4
“... of high levels of radiation-induced chromosomal damage in non-cycling A-T cells [19, 23], iii) the ability to uncouple certain ATM protein domains for their function in chromosomal radiosensitivity and cell cycle defects [22] and iv) the analyses of double mutant chicken DT40 cells, which demonstrate that aberrant…”
Background
Neocarzinostatin-induced Rad51 nuclear focus formation is cell cycle regulated and aberrant in AT cells
Yuan, S. F. (2003) · Toxicology and Applied Pharmacology · doi:10.1016/s0041-008x(03)00013-9 · Cited by 4
Spontaneous DNA-RNA hybrids: differential impacts throughout the cell cycle
Gómez‐González, B., Barroso, S. I., Herrera‐Moyano, E., & Aguilera, A. (2020) · Cell Cycle · doi:10.1080/15384101.2020.1728015 · Cited by 3
“The loss of the ATM/CHK2 kinase pathway likely reflects this situation in which DNA breaks are not efficiently handled by the cellular DNA repair machineries and remain unrepaired [29] leading to DNA-RNA hybrid accumulation [9].”
Background
Ataxia-Telangiectasia
Treuner, K., & Barlow, C. (2003) · Elsevier eBooks · doi:10.1016/b978-012566652-7/50023-x · Cited by 4
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Authors: Morrison, C., Sonoda, E., Takao, N., Shinohara, A., Yamamoto, K., & Takeda, S.
Affiliations: Kyoto University (JP)
Kanazawa University (JP)
University of Chicago (US)
Corresponding author: Takeda, Shunichi
ORCID: Morrison, Ciaran
Venue: The EMBO Journal
Publisher: Springer Science and Business Media LLC
Published: 2000-02-01
Volume: 19
Issue: 3
Pages: 463-471
ISSN: 0261-4189 (ISSN-L)
1460-2075
DOI: 10.1093/emboj/19.3.463
PMC: PMC305583
OpenAlex: W2017297714
Cited by: 312
References: 76
Citations by year: 2026: 6 · 2025: 1 · 2024: 10 · 2023: 2 · 2022: 8 · 2021: 6 · 2020: 9 · 2019: 8 · 2018: 9 · 2017: 9 · 2016: 1 · 2015: 12 · 2014: 9 · 2013: 8 · 2012: 15
FWCI: 10.74
Type: journal article
Language: en
Update notices: erratum (2000-02-15)
Open access: bronze
doi.org
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: The EMBO Journal (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Wellcome Trust
QIMR Berghofer Medical Research Institute
University of Cambridge
University of Sussex
Mochida Memorial Foundation for Medical and Pharmaceutical Research
Bayer Yakuhin
Medical Research Council
Japan Society for the Promotion of Science (CREST)
Core Research for Evolutional Science and Technology
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
Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
Keywords: ATM kinase, ataxia telangiectasia, homologous recombination, non-homologous end joining, DNA double-strand break repair, radiosensitivity, chromosomal instability, cell cycle checkpoints, RAD51, Rad54, Ku70, DT40 cells, chromosomal abnormalities
MeSH terms: Ku Autoantigen, Animals, Ataxia Telangiectasia, Cell Division, Cell Line, Chickens, Chromosome Aberrations, DNA Damage, DNA Repair, DNA Helicases, DNA-Binding Proteins, Fluorescent Antibody Technique, Fungal Proteins, Humans, Nuclear Proteins, Radiation Tolerance, Recombination, Genetic, Immunoblotting, Protein Serine-Threonine Kinases, Gene Targeting, Cell Cycle Proteins, Tumor Suppressor Proteins, Saccharomyces cerevisiae Proteins, Avian Proteins, Antigens, Nuclear, DNA Repair Enzymes, Rad51 Recombinase, Ataxia Telangiectasia Mutated Proteins

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The controlling role of ATM in homologous recombinational repair of DNA damage

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