ArticleCurrent biology : CB2019
A Genome-wide Screen Reveals that Reducing Mitochondrial DNA Polymerase Can Promote Elimination of Deleterious Mitochondrial Mutations.
Article in Current biology : CB, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed.
- Inheritance and selection of the mitochondrial genome.Nature reviews. Genetics · 2026Review
- Mitochondrial DNA Inheritance and Germline Purifying Selection: Insights FromAnnual review of genetics · 2026Review
- Distinct age-related pattern of mitochondrial somatic mutations across multiple sclerosis phenotypes.Journal of neurology · 2026Article
- Single-molecule mitochondrial DNA imaging reveals heteroplasmy dynamics shaped by developmental bottlenecks and selection in vivo.Developmental cell · 2026Article
- MitoPerturb-Seq identifies gene-specific single-cell responses to mitochondrial DNA depletion and heteroplasmy.Nature structural & molecular biology · 2026Article
- Trans-generational maintenance of mitochondrial DNA integrity in oocytes during early folliculogenesis.PLoS genetics · 2025Article
- Replication competition drives the selective mtDNA inheritance in Drosophila ovary.Cell reports · 2025Article
- Selfish mutations promote age-associated erosion of mtDNA integrity in mammals.Nature communications · 2025Article
- Selection promotes age-dependent degeneration of the mitochondrial genome.bioRxiv : the preprint server for biology · 2024Article
- Multiple distinct evolutionary mechanisms govern the dynamics of selfish mitochondrial genomes in Caenorhabditis elegans.Nature communications · 2024Article
- Maternal age enhances purifying selection on pathogenic mutations in complex I genes of mammalian mtDNA.Nature aging · 2024Article
- Challenges and opportunities to bridge translational to clinical research for personalized mitochondrial medicine.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- Review
- REC drives recombination to repair double-strand breaks in animal mtDNA.The Journal of cell biology · 2023Article
- The gender-specific impact of starvation on mitotypes diversity in adults ofOpen biology · 2022Article
- Mitigation of age-dependent accumulation of defective mitochondrial genomes.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- LONP-1 and ATFS-1 sustain deleterious heteroplasmy by promoting mtDNA replication in dysfunctional mitochondria.Nature cell biology · 2022Article
- Cellular mechanisms of mtDNA heteroplasmy dynamics.Critical reviews in biochemistry and molecular biology · 2021Review
- Mitochondrial function in development and disease.Disease models & mechanisms · 2021Review
- Mitochondrial DNA Dynamics in Reprogramming to Pluripotency.Trends in cell biology · 2021Review
Corrections and comments
- Commented on by
Authors and funding
4 authors.
Funding
Abstract
A mutant mitochondrial genome arising amid the pool of mitochondrial genomes within a cell must compete with existing genomes to survive to the next generation. Even weak selective forces can bias transmission of one genome over another to affect the inheritance of mitochondrial diseases and guide the evolution of mitochondrial DNA (mtDNA). Studies in several systems suggested that purifying selection in the female germline reduces transmission of detrimental mitochondrial mutations [1-7]. In contrast, some selfish genomes can take over despite a cost to host fitness [8-13]. Within individuals, the outcome of competition is therefore influenced by multiple selective forces. The nuclear genome, which encodes most proteins within mitochondria, and all external regulators of mitochondrial biogenesis and dynamics can influence the competition between mitochondrial genomes [14-18], yet little is known about how this works. Previously, we established a Drosophila line transmitting two mitochondrial genomes in a stable ratio enforced by purifying selection benefiting one genome and a selfish advantage favoring the other [8]. Here, to find nuclear genes that impact mtDNA competition, we screened heterozygous deletions tiling ∼70% of the euchromatic regions and examined their influence on this ratio. This genome-wide screen detected many nuclear modifiers of this ratio and identified one as the catalytic subunit of mtDNA polymerase gene (POLG), tam. A reduced dose of tam drove elimination of defective mitochondrial genomes. This study suggests that our approach will uncover targets for interventions that would block propagation of pathogenic mitochondrial mutations.
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.