ReviewIUBMB life2021
Not all mitochondrial DNAs are made equal and the nucleus knows it.
Review in IUBMB life, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 34 citations in OpenAlex.
- Optimized RNA-seq workflow for routine diagnosis of mitochondrial diseases using aberrant expression analysis and phenotype-driven prioritization.European journal of human genetics : EJHG · 2026Article
- Mitochondrial DNA regulation of hepatic ischemia-reperfusion injury and intervention strategies.Journal of translational medicine · 2026Review
- Phenogenomic resources immortalized in a panel of wild-derived strains of five species of house mice.Scientific reports · 2025Article
- Hypoxia-induced tRF-3Frontiers in pharmacology · 2025Article
- Recommendations for mitochondria transfer and transplantation nomenclature and characterization.Nature metabolism · 2025Review
- Gene Flow Between Populations With Highly Divergent Mitogenomes in the Australian Stingless Bee,Ecology and evolution · 2024Article
- Role of mitochondria in inflammatory lung diseases.Frontiers in pharmacology · 2024Review
- Vanadium Pentoxide Exposure Causes Strain-Dependent Changes in Mitochondrial DNA Heteroplasmy, Copy Number, and Lesions, but Not Nuclear DNA Lesions.International journal of molecular sciences · 2023Article
- Article
- Multifaceted mitochondria: moving mitochondrial science beyond function and dysfunction.Nature metabolism · 2023Review
- Article
- Pathological and Therapeutic Advances in Parkinson's Disease: Mitochondria in the Interplay.Journal of Alzheimer's disease : JAD · 2023Review
- Variant pathogenic prediction by locus variability: the importance of the current picture of evolution.European journal of human genetics : EJHG · 2022Article
- Heteroplasmy of Wild-Type Mitochondrial DNA Variants in Mice Causes Metabolic Heart Disease With Pulmonary Hypertension and Frailty.Circulation · 2022Article
- Role of Mitochondrial Nucleic Acid Sensing Pathways in Health and Patho-Physiology.Frontiers in cell and developmental biology · 2022Review
- Relevance of sex-differenced analyses in bioenergetics and nutritional studies.Frontiers in nutrition · 2022Article
- Targeting Mitochondrial OXPHOS and Their Regulatory Signals in Prostate Cancers.International journal of molecular sciences · 2021Review
- Mitochondria-Induced Immune Response as a Trigger for Neurodegeneration: A Pathogen from Within.International journal of molecular sciences · 2021Review
- Not all mitochondrial DNAs are made equal and the nucleus knows it.IUBMB life · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The oxidative phosphorylation (OXPHOS) system is the only structure in animal cells with components encoded by two genomes, maternally transmitted mitochondrial DNA (mtDNA), and biparentally transmitted nuclear DNA (nDNA). MtDNA-encoded genes have to physically assemble with their counterparts encoded in the nucleus to build together the functional respiratory complexes. Therefore, structural and functional matching requirements between the protein subunits of these molecular complexes are rigorous. The crosstalk between nDNA and mtDNA needs to overcome some challenges, as the nuclear-encoded factors have to be imported into the mitochondria in a correct quantity and match the high number of organelles and genomes per mitochondria that encode and synthesize their own components locally. The cell is able to sense the mito-nuclear match through changes in the activity of the OXPHOS system, modulation of the mitochondrial biogenesis, or reactive oxygen species production. This implies that a complex signaling cascade should optimize OXPHOS performance to the cellular-specific requirements, which will depend on cell type, environmental conditions, and life stage. Therefore, the mitochondria would function as a cellular metabolic information hub integrating critical information that would feedback the nucleus for it to respond accordingly. Here, we review the current understanding of the complex interaction between mtDNA and nDNA.
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.