ArticlePLoS genetics2017
Nucleotide pools dictate the identity and frequency of ribonucleotide incorporation in mitochondrial DNA.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed.
- Nucleotide salvage, genome instability, and potential therapeutic applications.Nucleic acids research · 2026Review
- Article
- The low endoribonuclease activity and lack of rNMP preference of human mitochondrial topoisomerase 1 protect against ribonucleotide-dependent deletions.Nucleic acids research · 2025Article
- Engineered mitochondria in diseases: mechanisms, strategies, and applications.Signal transduction and targeted therapy · 2025Review
- TEFM facilitates transition from RNA synthesis to DNA synthesis at H-strand replication origin of mtDNA.Communications biology · 2025Article
- DNA repair pathways in the mitochondria.DNA repair · 2025Review
- Distinct features of ribonucleotides within genomic DNA in Aicardi-Goutières syndrome ortholog mutants ofiScience · 2024Article
- Light-strand bias and enriched zones of embedded ribonucleotides are associated with DNA replication and transcription in the human-mitochondrial genome.Nucleic acids research · 2024Article
- Distinct features of ribonucleotides within genomic DNA in Aicardi-Goutières syndrome (AGS)-ortholog mutants ofbioRxiv : the preprint server for biology · 2023Article
- Dynamic Patterns of Mammalian Mitochondrial DNA Replication Uncovered Using SSiNGLe-5'ES.International journal of molecular sciences · 2023Article
- Determination of the Ribonucleotide Content of mtDNA Using Alkaline Gels.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Mitochondrial DNA Repair in Neurodegenerative Diseases and Ageing.International journal of molecular sciences · 2022Review
- RRM1 variants cause a mitochondrial DNA maintenance disorder via impaired de novo nucleotide synthesis.The Journal of clinical investigation · 2022Article
- Ribonucleotide Incorporation by Eukaryotic B-Family Replicases and Its Implications for Genome Stability.Annual review of biochemistry · 2022Review
- Mitochondrial DNA Instability in Mammalian Cells.Antioxidants & redox signaling · 2022Review
- Review
- MTBSTFA derivatization-LC-MS/MS approach for the quantitative analysis of endogenous nucleotides in human colorectal carcinoma cells.Journal of pharmaceutical analysis · 2022Article
- Ribonucleotides embedded in template DNA impair mitochondrial RNA polymerase progression.Nucleic acids research · 2022Article
- Remdesivir triphosphate blocks DNA synthesis and increases exonucleolysis by the replicative mitochondrial DNA polymerase, Pol γ.Mitochondrion · 2021Article
- Enhanced nucleotide analysis enables the quantification of deoxynucleotides in plants and algae revealing connections between nucleoside and deoxynucleoside metabolism.The Plant cell · 2021Article
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9 authors.
Funding
Abstract
Previous work has demonstrated the presence of ribonucleotides in human mitochondrial DNA (mtDNA) and in the present study we use a genome-wide approach to precisely map the location of these. We find that ribonucleotides are distributed evenly between the heavy- and light-strand of mtDNA. The relative levels of incorporated ribonucleotides reflect that DNA polymerase γ discriminates the four ribonucleotides differentially during DNA synthesis. The observed pattern is also dependent on the mitochondrial deoxyribonucleotide (dNTP) pools and disease-causing mutations that change these pools alter both the absolute and relative levels of incorporated ribonucleotides. Our analyses strongly suggest that DNA polymerase γ-dependent incorporation is the main source of ribonucleotides in mtDNA and argues against the existence of a mitochondrial ribonucleotide excision repair pathway in human cells. Furthermore, we clearly demonstrate that when dNTP pools are limiting, ribonucleotides serve as a source of building blocks to maintain DNA replication. Increased levels of embedded ribonucleotides in patient cells with disturbed nucleotide pools may contribute to a pathogenic mechanism that affects mtDNA stability and impair new rounds of mtDNA replication.
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