Regulation of DNA Repair Mechanisms: How the Chromatin Environment Regulates the DNA Damage Response
Open accessAbstract
Cellular DNA is constantly challenged by damage-inducing factors derived from exogenous or endogenous sources. In order to maintain genome stability and integrity, cells have evolved a wide variety of DNA repair pathways which counteract different types of DNA lesions, also referred to as the DNA damage response (DDR). However, DNA in eukaryotes is highly organized and compacted into chromatin representing major constraints for all cellular pathways, including DNA repair pathways, which require DNA as their substrate. Therefore, the chromatin configuration surrounding the lesion site undergoes dramatic remodeling to facilitate access of DNA repair factors and subsequent removal of the DNA lesion. In this review, we focus on the question of how the cellular DNA repair pathways overcome the chromatin barrier, how the chromatin environment is rearranged to facilitate efficient DNA repair, which proteins mediate this re-organization process and, consequently, how the altered chromatin landscape is involved in the regulation of DNA damage responses.
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Repair of damage both in GG-NER and TC-NER requires chromatin remodeling for enhanced access of pathway factors to existing damage.
“Repair of damage both in GG-NER and TC-NER requires chromatin remodeling for the enhanced access of pathway factors to existing damage.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [106]
The NER pathway in eukaryotes is tightly regulated by post-translational modifications and chromatin dynamics.
“Moreover the NER pathway in eukaryotes is tightly regulated by post-translational modifications and chromatin dynamics reviewed in [89,106,107,108,109].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [106]
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DNA Repair Defects in Sarcomas
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Martínez‐López, W., Moreno-Ortega, D., Valencia-Payan, J., Sammader, P., Meschini, R., & Palitti, F. (2018) · Mutation Research/Genetic Toxicology and Environmental Mutagenesis · doi:10.1016/j.mrgentox.2018.08.003 · Cited by 1 · see citing works
Emerging confluences of epigenetics and DNA repair in cancer and disease
Klein, C. B. (2019) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2019.108282 · Cited by 1 · see citing works
TET3 IMPACTS CARDIAC FIBROSIS PARTIALLY VIA REGULATION OF DNA DAMAGE RESPONSE
Rath, S. K. (2020) · doi:10.53846/goediss-7851 · Cited by 1 · see citing works
The PRC2.1 Subcomplex Opposes G1 Progression through Regulation of CCND1 and CCND2Preprint
Longhurst, A. D., Wang, K. E., Suresh, H. G., Ketavarapu, M., Ward, H. N., Jones, I. R., Narayan, V., Hundley, F. V., Hassan, A. Z., Boone, C. M., et al. (2024) · eLife · doi:10.7554/elife.97577.2 · Cited by 1 · see citing works
Heterogeneity in Nucleosome Spacing Governs Chromatin ElasticityPreprint
Beltran, B. G., Kannan, D., MacPherson, Q., & Spakowitz, A. J. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/708966
Neurodegeneração no Envelhecimento: Lições da Síndrome de Cockayne
Nascimento, L. L. S. (2022) · doi:10.11606/t.42.2022.tde-15082022-114300
The PRC2.1 subcomplex opposes G1 progression through regulation of CCND1 and CCND2
Longhurst, A. D., Wang, K. E., Suresh, H. G., Ketavarapu, M., Ward, H. N., Jones, I. R., Narayan, V., Hundley, F. V., Hassan, A. Z., Boone, C. M., et al. (2025) · eLife · doi:10.7554/elife.97577.3
Lypova, N., Dougherty, S. M., Clem, B. F., Feng, J. C., Yin, X., Zhang, X., Li, X., Chesney, J. A., & Imbert-Fernandez, Y. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.03.25.586703
Abdalla, O., & Walker, C. G. (2024) · Research Square · doi:10.21203/rs.3.rs-4342402/v1
The PRC2.1 Subcomplex Opposes G1 Progression through Regulation of CCND1 and CCND2Preprint
Longhurst, A. D., Wang, K. E., Suresh, H. G., Ketavarapu, M., Ward, H. N., Jones, I. R., Narayan, V., Hundley, F. V., Hassan, A. Z., Boone, C. M., et al. (2024) · eLife · doi:10.7554/elife.97577.1
Investigating the effects of ageing on DNA repair in mesenchymal stromal cells
Frommelt, T. (2024) · Queensland University of Technology · doi:10.5204/thesis.eprints.248588
Abdalla, O., & Walker, C. G. (2024) · Research Square · doi:10.21203/rs.3.rs-4342402/v2
Abdalla, O., & Walker, C. G. (2024) · Research Square · doi:10.21203/rs.3.rs-4342402/v3
- Authors
- Stadler, J., & Richly, H.
- Affiliations
- Johannes Gutenberg University Mainz (DE)
- Institute of Molecular Biology (DE)
- Corresponding author
- Richly, Holger
- ORCID
- Richly, Holger
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2017-08-05
- Volume
- 18
- Issue
- 8
- Pages
- 1715
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC5578105
- OpenAlex
- W2743728950
- Cited by
- 110
- References
- 102
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 18 · 2023: 13 · 2022: 12 · 2021: 14 · 2020: 20 · 2019: 13 · 2018: 10
- FWCI
- 1.10
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Boehringer Ingelheim Stiftung
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- DNA repair, DNA damage response, chromatin remodeling, chromatin environment, genome stability, DNA repair pathways, chromatin accessibility, DNA lesions
- MeSH terms
- Animals, Chromatin, DNA Damage, DNA Repair, Humans, Models, Biological, Phosphorylation, Ubiquitination
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