ArticleiScience2020
Optic Atrophy 1 Controls Human Neuronal Development by Preventing Aberrant Nuclear DNA Methylation.
Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Modelling mitochondrial diseases in neuronsJournal of neuromuscular diseases · 2025Pooled it
- Disrupted energy metabolism is associated with retinal ganglion cell degeneration in autosomal dominant optic atrophy.Science advances · 2026Article
- The synthetic cannabinoid THJ-2201 modulates mitochondrial activity and enhances mitochondrial recruitment to newly-forming neurites during neurodifferentiation of NG108-15 cells.Archives of toxicology · 2026Article
- The Synthetic Cannabinoid ADB-FUBINACA Disrupts Mitochondrial Morphology and Dynamics during Neuronal Differentiation of NG108-15 Cells.Molecular neurobiology · 2026Article
- Optic Atrophy 1: The Conductor of Cellular Harmony and Age-Related Pathologies.Aging and disease · 2025Review
- Loss of dynamin 1-like protein impairs mitochondrial function and self-renewal, and activates the integrated stress response in human embryonic stem cells.Frontiers in genetics · 2025Article
- WTAP-mediated mRedox report : communications in free radical research · 2024Article
- TAp73 regulates mitochondrial dynamics and multiciliated cell homeostasis through an OPA1 axis.Cell death & disease · 2024Article
- Differentiation activates mitochondrial OPA1 processing in myoblast cell lines.Mitochondrion · 2024Article
- OMA1-Mediated Mitochondrial Dynamics Balance Organellar Homeostasis Upstream of Cellular Stress Responses.International journal of molecular sciences · 2024Review
- The Neuroprotective Flavonoids Sterubin and Fisetin Maintain Mitochondrial Health under Oxytotic/Ferroptotic Stress and Improve Bioenergetic Efficiency in HT22 Neuronal Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Human retinal organoids with an OPA1 mutation are defective in retinal ganglion cell differentiation and function.Stem cell reports · 2024Article
- Modelling autosomal dominant optic atrophy associated with OPA1 variants in iPSC-derived retinal ganglion cells.Human molecular genetics · 2022Article
- CRISPR-Cas9 correction ofMolecular therapy. Nucleic acids · 2021Article
- Tau phosphorylation and OPA1 proteolysis are unrelated events: Implications for Alzheimer's Disease.Biochimica et biophysica acta. Molecular cell research · 2021Article
- Modelling Mitochondrial Disease in Human Pluripotent Stem Cells: What Have We Learned?International journal of molecular sciences · 2021Review
- Mitochondrial OPA1 cleavage is reversibly activated by differentiation of H9c2 cardiomyoblasts.Mitochondrion · 2021Article
- OMA1-An integral membrane protease?Biochimica et biophysica acta. Proteins and proteomics · 2021Review
- Review
- A Perspective on Accelerated Aging Caused by the Genetic Deficiency of the Metabolic Protein, OPA1.Frontiers in neurology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Optic atrophy 1 (OPA1), a GTPase at the inner mitochondrial membrane involved in regulating mitochondrial fusion, stability, and energy output, is known to be crucial for neural development: Opa1 heterozygous mice show abnormal brain development, and inactivating mutations in OPA1 are linked to human neurological disorders. Here, we used genetically modified human embryonic and patient-derived induced pluripotent stem cells and reveal that OPA1 haploinsufficiency leads to aberrant nuclear DNA methylation and significantly alters the transcriptional circuitry in neural progenitor cells (NPCs). For instance, expression of the forkhead box G1 transcription factor, which is needed for GABAergic neuronal development, is repressed in OPA1+/- NPCs. Supporting this finding, OPA1+/- NPCs cannot give rise to GABAergic interneurons, whereas formation of glutamatergic neurons is not affected. Taken together, our data reveal that OPA1 controls nuclear DNA methylation and expression of key transcription factors needed for proper neural cell specification.
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.