ArticleGenes & development2012
mtDNA lineage analysis of mouse L-cell lines reveals the accumulation of multiple mtDNA mutants and intermolecular recombination.
Article in Genes & development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Single-cell Omics Assessment of Mitochondrial Function: Current Status and Future Perspectives.Genomics, proteomics & bioinformatics · 2026Review
- A scalable embryonic stem cell-based platform for efficient generation of mitochondrial DNA mutant mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Routine mitochondrial recombination drives rapid concerted evolution of duplicated control regions in a wild fish.Heredity · 2026Article
- Estrogen-related receptors regulate innate and adaptive muscle mitochondrial energetics through cooperative and distinct actions.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- REC drives recombination to repair double-strand breaks in animal mtDNA.The Journal of cell biology · 2023Article
- Cancer Cell Culture: The Basics and Two-Dimensional Cultures.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Emerging Roles of NDUFS8 Located in Mitochondrial Complex I in Different Diseases.Molecules (Basel, Switzerland) · 2022Review
- Embryo and Its Mitochondria.Antioxidants (Basel, Switzerland) · 2021Review
- Mitochondrial Haplotype of the Host Stromal Microenvironment Alters Metastasis in a Non-cell Autonomous Manner.Cancer research · 2020Article
- ERRγ Promotes Angiogenesis, Mitochondrial Biogenesis, and Oxidative Remodeling in PGC1α/β-Deficient Muscle.Cell reports · 2018Article
- Mitochondrial dysfunction and mitochondrial dynamics-The cancer connection.Biochimica et biophysica acta. Bioenergetics · 2017Review
- Uniparental Inheritance Promotes Adaptive Evolution in Cytoplasmic Genomes.Molecular biology and evolution · 2017Article
- Notch activation drives adipocyte dedifferentiation and tumorigenic transformation in mice.The Journal of experimental medicine · 2016Article
- Oncolytic adenovirus targeting cyclin E overexpression repressed tumor growth in syngeneic immunocompetent mice.BMC cancer · 2015Article
- Mitochondrial retrograde signaling induces epithelial-mesenchymal transition and generates breast cancer stem cells.Oncogene · 2014Article
- Intraclonal recovery of 'slow clones'-a manifestation of genomic instability: are mitochondria the key to an explanation?Radiation and environmental biophysics · 2014Review
- No recombination of mtDNA after heteroplasmy for 50 generations in the mouse maternal germline.Nucleic acids research · 2014Article
- Mitochondrial DNA genetics and the heteroplasmy conundrum in evolution and disease.Cold Spring Harbor perspectives in biology · 2013Review
- Mitochondrial retrograde signaling at the crossroads of tumor bioenergetics, genetics and epigenetics.Mitochondrion · 2013Review
- Plastid genome instability leads to reactive oxygen species production and plastid-to-nucleus retrograde signaling in Arabidopsis.Plant physiology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The role of mitochondrial DNA (mtDNA) mutations and mtDNA recombination in cancer cell proliferation and developmental biology remains controversial. While analyzing the mtDNAs of several mouse L cell lines, we discovered that every cell line harbored multiple mtDNA mutants. These included four missense mutations, two frameshift mutations, and one tRNA homopolymer expansion. The LA9 cell lines lacked wild-type mtDNAs but harbored a heteroplasmic mixture of mtDNAs, each with a different combination of these variants. We isolated each of the mtDNAs in a separate cybrid cell line. This permitted determination of the linkage phase of each mtDNA and its physiological characteristics. All of the polypeptide mutations inhibited their oxidative phosphorylation (OXPHOS) complexes. However, they also increased mitochondrial reactive oxygen species (ROS) production, and the level of ROS production was proportional to the cellular proliferation rate. By comparing the mtDNA haplotypes of the different cell lines, we were able to reconstruct the mtDNA mutational history of the L-L929 cell line. This revealed that every heteroplasmic L-cell line harbored a mtDNA that had been generated by intracellular mtDNA homologous recombination. Therefore, deleterious mtDNA mutations that increase ROS production can provide a proliferative advantage to cancer or stem cells, and optimal combinations of mutant loci can be generated through recombination.
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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.