ArticleScience advances2025
Allele frequency selection and no age-related increase in human oocyte mitochondrial mutations.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Maternal age as a driver of genome instability: mechanisms linking aneuploidy, mutagenesis and mitochondrial dysfunction.Archives of toxicology · 2026Review
- Inheritance and selection of the mitochondrial genome.Nature reviews. Genetics · 2026Review
- Nuclear mitochondrial sequences in great ape telomere-to-telomere genomes.Genome research · 2026Article
- Endocrine and Molecular Mechanisms of Oocyte Aging: From Gonadotropin Signaling to Metabolic and Microenvironmental Dysfunction.Current issues in molecular biology · 2026Review
- Mapping ovarian cellular and molecular landscape across the lifespan of women: a scoping review.Human reproduction update · 2026Article
- Mammalian mitochondrial DNA accumulates insertions and deletions with age in energetically demanding tissues.Molecular biology and evolution · 2026Article
- Detection of mutations: from Ames test to duplex sequencing.Frontiers in molecular biosciences · 2026Review
- Understanding the impact of mitochondrial DNA mutations on aging and carcinogenesis (Review).International journal of molecular medicine · 2025Review
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9 authors.
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Abstract
Mitochondria, cellular powerhouses, harbor DNA [mitochondrial DNA (mtDNA)] inherited from the mothers. mtDNA mutations can cause diseases, yet whether they increase with age in human oocytes remains understudied. Here, using highly accurate duplex sequencing, we detected de novo mutations in single oocytes, blood, and saliva in women 20 to 42 years of age. We found that, with age, mutations increased in blood and saliva but not in oocytes. In oocytes, mutations with high allele frequencies were less prevalent in coding than noncoding regions, whereas mutations with low allele frequencies were more uniformly distributed along the mtDNA, suggesting frequency-dependent purifying selection. Thus, mtDNA in human oocytes is protected against accumulation of mutations with aging and having functional consequences. These findings are particularly timely as humans tend to reproduce later in life.
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