ArticlePLoS computational biology2015
Context-Dependent Role of Mitochondrial Fusion-Fission in Clonal Expansion of mtDNA Mutations.
Article in PLoS computational biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 70 citations in OpenAlex.
- Optimal Organelle Inheritance Strategies Under Different Changing Environments and Mutational Pressures.Genome biology and evolution · 2026Article
- SBK3 suppresses angiotensin II-induced cardiac hypertrophy by regulating mitochondrial metabolism.Scientific reports · 2025Article
- Molecular mechanisms of mitochondrial dynamics.Nature reviews. Molecular cell biology · 2025Review
- Dissecting the sequential evolution of a selfish mitochondrial genome in Caenorhabditis elegans.Heredity · 2024Article
- Evolution and maintenance of mtDNA gene content across eukaryotes.The Biochemical journal · 2024Review
- 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
- Mitochondrial DNA Repair in Neurodegenerative Diseases and Ageing.International journal of molecular sciences · 2022Review
- An explanation of how mutant and wild-type mitochondria might stably co-exist in inherited mitochondrial diseases.PNAS nexus · 2022Article
- Exchange on dynamic encounter networks allows plant mitochondria to collect complete sets of mitochondrial DNA products despite their incomplete genomes.Quantitative plant biology · 2022Article
- Mitochondrial DNA Release Contributes to Intestinal Ischemia/Reperfusion Injury.Frontiers in pharmacology · 2022Review
- The mtDNA mutation spectrum in the PolG mutator mouse reveals germline and somatic selection.BMC genomic data · 2021Article
- Thermodynamic analysis of DNA hybridization signatures near mitochondrial DNA deletion breakpoints.iScience · 2021Article
- Functions of outer mitochondrial membrane proteins: mediating the crosstalk between mitochondrial dynamics and mitophagy.Cell death and differentiation · 2021Review
- MtDNA sequence features associated with 'selfish genomes' predict tissue-specific segregation and reversion.Nucleic acids research · 2020Article
- Network Simulations Reveal Molecular Signatures of Vulnerability to Age-Dependent Stress and Tau Accumulation.Frontiers in molecular biosciences · 2020Article
- Evolving mtDNA populations within cells.Biochemical Society transactions · 2019Review
- Mitochondrial Network State Scales mtDNA Genetic DynamicsGenetics · 2019Article
- Selfish Mitonuclear Conflict.Current biology : CB · 2019Review
- A battle for transmission: the cooperative and selfish animal mitochondrial genomes.Open biology · 2019Review
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The accumulation of mutant mitochondrial DNA (mtDNA) molecules in aged cells has been associated with mitochondrial dysfunction, age-related diseases and the ageing process itself. This accumulation has been shown to often occur clonally, where mutant mtDNA grow in number and overpopulate the wild-type mtDNA. However, the cell possesses quality control (QC) mechanisms that maintain mitochondrial function, in which dysfunctional mitochondria are isolated and removed by selective fusion and mitochondrial autophagy (mitophagy), respectively. The aim of this study is to elucidate the circumstances related to mitochondrial QC that allow the expansion of mutant mtDNA molecules. For the purpose of the study, we have developed a mathematical model of mitochondrial QC process by extending our previous validated model of mitochondrial turnover and fusion-fission. A global sensitivity analysis of the model suggested that the selectivity of mitophagy and fusion is the most critical QC parameter for clearing de novo mutant mtDNA molecules. We further simulated several scenarios involving perturbations of key QC parameters to gain a better understanding of their dynamic and synergistic interactions. Our model simulations showed that a higher frequency of mitochondrial fusion-fission can provide a faster clearance of mutant mtDNA, but only when mutant-rich mitochondria that are transiently created are efficiently prevented from re-fusing with other mitochondria and selectively removed. Otherwise, faster fusion-fission quickens the accumulation of mutant mtDNA. Finally, we used the insights gained from model simulations and analysis to propose a possible circumstance involving deterioration of mitochondrial QC that permits mutant mtDNA to expand with age.
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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.