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Human cells are protected from mitochondrial dysfunction by complementation of DNA products in fused mitochondria
Abstract
Extensive complementation between fused mitochondria is indicated by recombination of 'parental' mitochondrial (mt) DNA (ref. 1,2) of yeast and plant cells. It has been difficult, however, to demonstrate the occurrence of complementation between fused mitochondria in mammalian species through the presence of recombinant mtDNA molecules, because sequence of mtDNA throughout an individual tends to be uniform owing to its strictly maternal inheritance. We isolated two types of respiration-deficient cell lines, with pathogenic mutations in mitochondrial tRNAIle or tRNALeu(UUR) genes from patients with mitochondrial diseases. The coexistence of their mitochondria within hybrids restored their normal morphology and respiratory enzyme activity by 10-14 days after fusion, indicating the presence of an extensive and continuous exchange of genetic contents between the mitochondria. This complementation between fused mitochondria may represent a defence of highly oxidative organelles against mitochondrial dysfunction caused by the accumulation of mtDNA lesions with age.
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“This process enables the redistribution of energy in the form of mitochondrial potential, metabolites, proteins, and mtDNA, improving calcium handling, and ATP synthesis [24, 54–57].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [57]
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Bess, A. S. (2012) · DukeSpace (Duke University)
Lukyanova, L. D., Germanova, E. L., Khmil, N. V., Pavlik, L. L., Mikheeva, I. B., Shigaeva, M. I., & Mironova, G. D. (2023) · Vide Leaf, Hyderabad eBooks · doi:10.37247/pamol4ed.4.23.11
Impact of Mitochondrial Fission and Fusion on Neuronal Health and Incidence of Dementia
Holt, A. G., & Davies, A. M. (2026) · Clinical bioenergetics · doi:10.3390/clinbioenerg2030012
Metadata
- Authors
- Ono, T., Isobe, K., Nakada, K., & Hayashi, J.-I.
- Affiliations
- University of Tsukuba (JP)
- Corresponding author
- Hayashi, Jun-Ichi
- ORCID
- Nakada, Kazuto
- Venue
- Nature Genetics
- Published
- 2001-07
- Volume
- 28
- Issue
- 3
- Pages
- 272-275
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- OpenAlex
- W1554250492
- Cited by
- 420
- References
- 29
- Citations by year
- 2026: 7 · 2025: 14 · 2024: 14 · 2023: 10 · 2022: 16 · 2021: 24 · 2020: 18 · 2019: 15 · 2018: 10 · 2017: 24 · 2016: 13 · 2015: 21 · 2014: 21 · 2013: 11 · 2012: 28
- FWCI
- 5.94
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- mitochondrial fusion, mitochondrial recombination, mitochondrial dysfunction, mitochondrial tRNA mutations, mitochondrial disease, respiratory deficiency, oxidative stress, human cell lines
- MeSH terms
- DNA, Mitochondrial, Genetic Complementation Test, Humans, Hybrid Cells, Intracellular Membranes, Membrane Fusion, Mitochondria, Oxygen Consumption, RNA, Transfer, Ile, RNA, Transfer, Leu, Mitochondrial Myopathies
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