ArticleAmerican journal of human genetics2016
Evolution of Cell-to-Cell Variability in Stochastic, Controlled, Heteroplasmic mtDNA Populations.
Article in American journal of human genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Optimal Organelle Inheritance Strategies Under Different Changing Environments and Mutational Pressures.Genome biology and evolution · 2026Article
- Article
- Evolution and maintenance of mtDNA gene content across eukaryotes.The Biochemical journal · 2024Review
- High-throughput single-cell analysis reveals progressive mitochondrial DNA mosaicism throughout life.Science advances · 2023Article
- Article
- Mitochondrial network structure controls cell-to-cell mtDNA variability generated by cell divisions.PLoS computational biology · 2023Article
- Stochastic survival of the densest and mitochondrial DNA clonal expansion in aging.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- Heteroplasmy of Wild-Type Mitochondrial DNA Variants in Mice Causes Metabolic Heart Disease With Pulmonary Hypertension and Frailty.Circulation · 2022Article
- Avoiding organelle mutational meltdown across eukaryotes with or without a germline bottleneck.PLoS biology · 2021Article
- Human pluripotent stem-cell-derived alveolar organoids for modeling pulmonary fibrosis and drug testing.Cell death discovery · 2021Article
- Not all mitochondrial DNAs are made equal and the nucleus knows it.IUBMB life · 2021Review
- MtDNA sequence features associated with 'selfish genomes' predict tissue-specific segregation and reversion.Nucleic acids research · 2020Article
- Cell identity and nucleo-mitochondrial genetic context modulate OXPHOS performance and determine somatic heteroplasmy dynamics.Science advances · 2020Article
- The rise and rise of mitochondrial DNA mutations.Open biology · 2020Review
- Pronounced somatic bottleneck in mitochondrial DNA of human hair.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Article
- Regulation of Mother-to-Offspring Transmission of mtDNA Heteroplasmy.Cell metabolism · 2019Article
- Evolving mtDNA populations within cells.Biochemical Society transactions · 2019Review
- Mitochondrial Network State Scales mtDNA Genetic DynamicsGenetics · 2019Article
- Energetic costs of cellular and therapeutic control of stochastic mitochondrial DNA populations.PLoS computational biology · 2019Article
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2 authors.
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Abstract
Populations of physiologically vital mitochondrial DNA (mtDNA) molecules evolve in cells under control from the nucleus. The evolution of populations of mixed mtDNA types is complicated and poorly understood, and variability of these controlled admixtures plays a central role in the inheritance and onset of genetic disease. Here, we develop a mathematical theory describing the evolution of, and variability in, these stochastic populations for any type of cellular control, showing that cell-to-cell variability in mtDNA and mutant load inevitably increases with time, according to rates that we derive and which are notably independent of the mechanistic details of feedback signaling. We show with a set of experimental case studies that this theory explains disparate quantitative results from classical and modern experimental and computational research on heteroplasmy variance in different species. We demonstrate that our general model provides a host of specific insights, including a modification of the often-used but hard-to-interpret Wright formula to correspond directly to biological observables, the ability to quantify selective and mutational pressure in mtDNA populations, and characterization of the pronounced variability inevitably arising from the action of possible mtDNA quality-control mechanisms. Our general theoretical framework, supported by existing experimental results, thus helps us to understand and predict the evolution of stochastic mtDNA populations in cell biology.
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