ArticleeLife2022
Genetically controlled mtDNA deletions prevent ROS damage by arresting oxidative phosphorylation.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- In the absence of mitochondrial fusion unequal segregation of mitochondria drives mtDNA loss.EMBO reports · 2026Article
- Reproductive Isolation due to Divergent Ecological Selection Is Accompanied by Vast Genomic Instability in Experimentally Evolved Yeast Populations.Molecular ecology · 2025Article
- Mechanism Analysis of UCP2 During the Oxidative Stress Injury of Intestinal Porcine Epithelial Cell Line-J2.Animals : an open access journal from MDPI · 2025Article
- Mitochondria-Nuclear Crosstalk: Orchestrating mtDNA Maintenance.Environmental and molecular mutagenesis · 2025Review
- Inheritance bias of deletion-harbouring mtDNA in yeast: The role of copy number and intracellular selection.PLoS genetics · 2025Article
- Analysis and identification of mitochondria-related genes associated with age-related hearing loss.BMC genomics · 2025Article
- Mitochondrial Genome Instability inBiology · 2024Article
- Highly parallelized laboratory evolution of wine yeasts for enhanced metabolic phenotypes.Molecular systems biology · 2024Article
- Mitochondrial complex I subunitHeliyon · 2024Review
- Mitochondrial Dysfunction as the Major Basis of Brain Aging.Biomolecules · 2024Review
- Spontaneous Mutations inInternational journal of molecular sciences · 2023Article
- Genome instability footprint under rapamycin and hydroxyurea treatments.PLoS genetics · 2023Article
- Global Transcriptomic Changes Elicited byJournal of fungi (Basel, Switzerland) · 2023Article
- Spontaneous Mutation Rates and Spectra of Respiratory-Deficient Yeast.Biomolecules · 2023Article
- Mapping mitonuclear epistasis using a novel recombinant yeast population.PLoS genetics · 2023Article
- Role of reactive oxygen species and mitochondrial damage in rheumatoid arthritis and targeted drugs.Frontiers in immunology · 2023Review
- Mitochondrial heteroplasmy as a cause of cell-to-cell phenotypic heterogeneity in clonal populations.Frontiers in cell and developmental biology · 2023Article
- Understanding Long COVID; Mitochondrial Health and Adaptation-Old Pathways, New Problems.Biomedicines · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deletion of mitochondrial DNA in eukaryotes is currently attributed to rare accidental events associated with mitochondrial replication or repair of double-strand breaks. We report the discovery that yeast cells arrest harmful intramitochondrial superoxide production by shutting down respiration through genetically controlled deletion of mitochondrial oxidative phosphorylation genes. We show that this process critically involves the antioxidant enzyme superoxide dismutase 2 and two-way mitochondrial-nuclear communication through Rtg2 and Rtg3. While mitochondrial DNA homeostasis is rapidly restored after cessation of a short-term superoxide stress, long-term stress causes maladaptive persistence of the deletion process, leading to complete annihilation of the cellular pool of intact mitochondrial genomes and irrevocable loss of respiratory ability. This shows that oxidative stress-induced mitochondrial impairment may be under strict regulatory control. If the results extend to human cells, the results may prove to be of etiological as well as therapeutic importance with regard to age-related mitochondrial impairment and disease.
Indexed as
Identifiers
What OpenQuestion holds
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.