Low doses of ultraviolet radiation and oxidative damage induce dramatic accumulation of mitochondrial DNA replication intermediates, fork regression, and replication initiation shift
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Mitochondrial DNA is prone to damage by various intrinsic as well as environmental stressors. DNA damage can in turn cause problems for replication, resulting in replication stalling and double-strand breaks, which are suspected to be the leading cause of pathological mtDNA rearrangements. In this study, we exposed cells to subtle levels of oxidative stress or UV radiation and followed their effects on mtDNA maintenance. Although the damage did not influence mtDNA copy number, we detected a massive accumulation of RNA:DNA hybrid–containing replication intermediates, followed by an increase in cruciform DNA molecules, as well as in bidirectional replication initiation outside of the main replication origin, O H. Our results suggest that mitochondria maintain two different types of replication as an adaptation to different cellular environments; the RNA:DNA hybrid–involving replication mode maintains mtDNA integrity in tissues with low oxidative stress, and the potentially more error tolerant conventional strand-coupled replication operates when stress is high.
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SSBs and DSBs generated as products of replication stalling, ROS activity and abortive topoisomerase action may be repaired by either HR or NHEJ.
“Furthermore, SSBs and DSBs generated as products of replication stalling, ROS activity and abortive topoisomerase action may be repaired by either HR or NHEJ [142,143].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [143]
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- Authors
- Torregrosa-Muñumer, R., Goffart, S., Haikonen, J. A., & Pohjoismäki, J. L. O.
- Affiliations
- Department of Biology, University of Eastern Finland, 80101 Joensuu, Finland
- University of Eastern Finland (FI)
- Corresponding author
- Pohjoismäki, Jaakko L. O.
- Venue
- Molecular Biology of the Cell
- Published
- 2015-11-15
- Volume
- 26
- Issue
- 23
- Pages
- 4197-4208
- ISSN
- 1059-1524 (ISSN-L)
- 1939-4586
- PMC
- PMC4642854
- OpenAlex
- W2278293559
- Cited by
- 42
- References
- 44
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 6 · 2020: 3 · 2019: 7 · 2018: 5 · 2017: 4 · 2016: 3
- FWCI
- 1.74
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by-nc-sa
- Locations
- Molecular Biology of the Cell (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
- Keywords
- mitochondrial DNA replication, ultraviolet radiation, oxidative stress, replication intermediates, RNA-DNA hybrids, cruciform DNA, replication fork regression, mitochondrial DNA copy number, mtDNA rearrangements, bidirectional replication, mitochondrial DNA damage
- MeSH terms
- Cells, Cultured, DNA Damage, DNA Repair, DNA Replication, DNA, Mitochondrial, Dose-Response Relationship, Radiation, Humans, Nucleic Acid Hybridization, RNA, Ultraviolet Rays, Oxidative Stress, Replication Origin, DNA Copy Number Variations, HEK293 Cells
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