ArticleNucleic acids research2022
A mitochondria-specific mutational signature of aging: increased rate of A > G substitutions on the heavy strand.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 41 citations in OpenAlex.
- Lifespan Predicts Mitochondrial Substitution Rates across Vertebrates, but Methodology Matters.Genome biology and evolution · 2026Article
- Allele frequency selection and no age-related increase in human oocyte mitochondrial mutations.Science advances · 2025Article
- Flipping the switch on some of the slowest mutating genomes: Direct measurements of plant mitochondrial and plastid mutation rates in msh1 mutants.PLoS genetics · 2025Article
- Deciphering the Foundations of Mitochondrial Mutational Spectra: Replication-Driven and Damage-Induced Signatures Across Chordate Classes.Molecular biology and evolution · 2025Article
- Flipping the switch on some of the slowest mutating genomes: Direct measurements of plant mitochondrial and plastid mutation rates inbioRxiv : the preprint server for biology · 2025Article
- Somatic mutations in aging and disease.GeroScience · 2024Review
- NeMu: a comprehensive pipeline for accurate reconstruction of neutral mutation spectra from evolutionary data.Nucleic acids research · 2024Article
- Metastatic pattern of ovarian cancer delineated by tracing the evolution of mitochondrial DNA mutations.Experimental & molecular medicine · 2023Article
- Secondary structure of the human mitochondrial genome affects formation of deletions.BMC biology · 2023Article
- Article
- The quality of human eggs and its pre-IVF incubation.Reproductive medicine and biologyReview
Corrections and comments
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Authors and funding
30 authors at 11 institutions in 7 countries.
Funding
Abstract
The mutational spectrum of the mitochondrial DNA (mtDNA) does not resemble any of the known mutational signatures of the nuclear genome and variation in mtDNA mutational spectra between different organisms is still incomprehensible. Since mitochondria are responsible for aerobic respiration, it is expected that mtDNA mutational spectrum is affected by oxidative damage. Assuming that oxidative damage increases with age, we analyse mtDNA mutagenesis of different species in regards to their generation length. Analysing, (i) dozens of thousands of somatic mtDNA mutations in samples of different ages (ii) 70053 polymorphic synonymous mtDNA substitutions reconstructed in 424 mammalian species with different generation lengths and (iii) synonymous nucleotide content of 650 complete mitochondrial genomes of mammalian species we observed that the frequency of AH > GH substitutions (H: heavy strand notation) is twice bigger in species with high versus low generation length making their mtDNA more AH poor and GH rich. Considering that AH > GH substitutions are also sensitive to the time spent single-stranded (TSSS) during asynchronous mtDNA replication we demonstrated that AH > GH substitution rate is a function of both species-specific generation length and position-specific TSSS. We propose that AH > GH is a mitochondria-specific signature of oxidative damage associated with both aging and TSSS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.