ArticlePLoS genetics2014
Oxidative stress is not a major contributor to somatic mitochondrial DNA mutations.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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Who cites it
107 citing papers in PubMed, 173 citations in OpenAlex.
- Low frequency mitochondrial DNA heteroplasmy SNPs in blood, retina, and [RPE+choroid] of age-related macular degeneration subjects.PloS one · 2021Trial
- Inheritance and selection of the mitochondrial genome.Nature reviews. Genetics · 2026Review
- Article
- Persistence of large mtDNA rearrangements linked to premature aging in Pol γ exonuclease-deficient mice.Nucleic acids research · 2026Article
- High-concentration MEHP triggers mtDNA depletion in undifferentiated HepaRG and C2C12 cultures and disrupts mitochondrial homeostasis in both HepaRG culture states.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Move beyond free radical theory of aging.iMetaOmics · 2026Review
- Mitochondrial DNA Replication and Disease: A Historical Perspective on Molecular Insights and Therapeutic Advances.International journal of molecular sciences · 2025Review
- Ligase 3 prevents oxidative strand break-induced mitochondrial DNA loss but is not essential for replicative circularization.Nucleic acids research · 2025Article
- Understanding the impact of mitochondrial DNA mutations on aging and carcinogenesis (Review).International journal of molecular medicine · 2025Review
- Disruption of recombination machinery alters the mutational landscape in plant organellar genomes.G3 (Bethesda, Md.) · 2025Article
- Revisiting the Role of Mitochondrial DNA Mutations in Aging: Bridging Theoretical Expectations with Empirical Observations.Aging and disease · 2025Review
- A Comprehensive Review of the Contribution of Mitochondrial DNA Mutations and Dysfunction in Polycystic Ovary Syndrome, Supported by Secondary Database Analysis.International journal of molecular sciences · 2025Review
- Unraveling the ROS-Inflammation-Immune Balance: A New Perspective on Aging and Disease.Aging and disease · 2025Review
- Aging through the lens of mitochondrial DNA mutations and inheritance paradoxes.Biogerontology · 2024Review
- Preventing excessive autophagy protects from the pathology of mtDNA mutations in Drosophila melanogaster.Nature communications · 2024Article
- Maintaining mitochondrial DNA copy number mitigates ROS-induced oocyte decline and female reproductive aging.Communications biology · 2024Article
- Evolution and maintenance of mtDNA gene content across eukaryotes.The Biochemical journal · 2024Review
- Disruption of recombination machinery alters the mutational landscape in plant organellar genomes.bioRxiv : the preprint server for biology · 2024Article
- A complete workflow for single cell mtDNAseq in CHO cells, from cell culture to bioinformatic analysis.Frontiers in bioengineering and biotechnology · 2024Article
- The Fate of Oxidative Strand Breaks in Mitochondrial DNA.Antioxidants (Basel, Switzerland) · 2023Article
47 more citing papers are in PubMed but not listed here.
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8 authors at 3 institutions in 1 country.
Funding
Abstract
The accumulation of somatic mitochondrial DNA (mtDNA) mutations is implicated in aging and common diseases of the elderly, including cancer and neurodegenerative disease. However, the mechanisms that influence the frequency of somatic mtDNA mutations are poorly understood. To develop a simple invertebrate model system to address this matter, we used the Random Mutation Capture (RMC) assay to characterize the age-dependent frequency and distribution of mtDNA mutations in the fruit fly Drosophila melanogaster. Because oxidative stress is a major suspect in the age-dependent accumulation of somatic mtDNA mutations, we also used the RMC assay to explore the influence of oxidative stress on the somatic mtDNA mutation frequency. We found that many of the features associated with mtDNA mutations in vertebrates are conserved in Drosophila, including a comparable somatic mtDNA mutation frequency (∼10(-5)), an increased frequency of mtDNA mutations with age, and a prevalence of transition mutations. Only a small fraction of the mtDNA mutations detected in young or old animals were G∶C to T∶A transversions, a signature of oxidative damage, and loss-of-function mutations in the mitochondrial superoxide dismutase, Sod2, had no detectable influence on the somatic mtDNA mutation frequency. Moreover, a loss-of-function mutation in Ogg1, which encodes a DNA repair enzyme that removes oxidatively damaged deoxyguanosine residues (8-hydroxy-2'-deoxyguanosine), did not significantly influence the somatic mtDNA mutation frequency of Sod2 mutants. Together, these findings indicate that oxidative stress is not a major cause of somatic mtDNA mutations. Our data instead suggests that somatic mtDNA mutations arise primarily from errors that occur during mtDNA replication. Further studies using Drosophila should aid in the identification of factors that influence the frequency of somatic mtDNA mutations.
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