ArticleEMBO molecular medicine2021
High-throughput screening identifies suppressors of mitochondrial fragmentation in OPA1 fibroblasts.
Article in EMBO molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 62 citations in OpenAlex.
- Mitochondrial dynamics in environmental neurotoxicity: beyond oxidative stress toward spatial and functional reorganization.Archives of toxicology · 2026Review
- Valproic acid remodels phosphatidylglycerol homeostasis and epithelial-macrophage crosstalk in inflammatory signaling.iScience · 2026Article
- Lipidomics Based on HILIC-ESI-HRMS Reveal Subtle Changes in the Mitochondrial Phospholipidome of Mouse Embryonic Fibroblasts Expressing Pathogenic Variants of Human OPA1 Protein.Molecules (Basel, Switzerland) · 2026Article
- Super-Refractory Status Epilepticus (SRSE) in a Patient With Compound Heterozygous OPA1 Variants: Case Report and Literature Review.Annals of clinical and translational neurology · 2026Review
- Mutant CHCHD10 disrupts cytochrome c oxidation and activates mitochondrial retrograde signaling.EMBO molecular medicine · 2026Article
- Microbial metabolite indole-3-propionic acid drives mitochondrial respiration in CD4Nature metabolism · 2025Article
- BMAL1 modulation alleviates inflammatory responses in monocytes by targeting the Fis1-mediated mitochondrial unfolded protein response in high-altitude hypoxia.Cell communication and signaling : CCS · 2025Article
- Mitochondrial Antiviral Signaling Protein Activation by Retinoic Acid-Inducible Gene I Agonist Triggers Potent Antiviral Defense in Umbilical Cord Mesenchymal Stromal Cells Without Compromising Mitochondrial Function.International journal of molecular sciences · 2025Article
- Disruption of mitochondrial homeostasis and permeability transition pore opening in OPA1 iPSC-derived retinal ganglion cells.Acta neuropathologica communications · 2025Article
- Molecular mechanisms of mitochondrial dynamics.Nature reviews. Molecular cell biology · 2025Review
- Dynamic label-free analysis of SARS-CoV-2 infection reveals virus-induced subcellular remodeling.Nature communications · 2024Article
- Lipidomics reveals the reshaping of the mitochondrial phospholipid profile in cells lacking OPA1 and mitofusins.Journal of lipid research · 2024Article
- KAT8 compound inhibition inhibits the initial steps of PINK1-dependant mitophagy.Scientific reports · 2024Article
- Spinning Disk Confocal Microscopy for Optimized and Quantified Live Imaging of 3D Mitochondrial Network.International journal of molecular sciences · 2024Article
- ATF4-dependent increase in mitochondrial-endoplasmic reticulum tethering following OPA1 deletion in skeletal muscle.Journal of cellular physiology · 2024Article
- Slowing reproductive ageing by preserving BCAT-1.Nature metabolism · 2024Article
- New insights into the role of mitochondrial metabolic dysregulation and immune infiltration in septic cardiomyopathy by integrated bioinformatics analysis and experimental validation.Cellular & molecular biology letters · 2024Article
- Mtfp1 ablation enhances mitochondrial respiration and protects against hepatic steatosis.Nature communications · 2023Article
- OPA1 Dominant Optic Atrophy: Pathogenesis and Therapeutic Targets.Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society · 2023Article
- Discovery of Potent Allosteric DRP1 Inhibitors by Disrupting Protein-Protein Interaction with MiD49.ACS medicinal chemistry letters · 2023Article
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
Mutations in OPA1 cause autosomal dominant optic atrophy (DOA) as well as DOA+, a phenotype characterized by more severe neurological deficits. OPA1 deficiency causes mitochondrial fragmentation and also disrupts cristae, respiration, mitochondrial DNA (mtDNA) maintenance, and cell viability. It has not yet been established whether phenotypic severity can be modulated by genetic modifiers of OPA1. We screened the entire known mitochondrial proteome (1,531 genes) to identify genes that control mitochondrial morphology using a first-in-kind imaging pipeline. We identified 145 known and novel candidate genes whose depletion promoted elongation or fragmentation of the mitochondrial network in control fibroblasts and 91 in DOA+ patient fibroblasts that prevented mitochondrial fragmentation, including phosphatidyl glycerophosphate synthase (PGS1). PGS1 depletion reduces CL content in mitochondria and rebalances mitochondrial dynamics in OPA1-deficient fibroblasts by inhibiting mitochondrial fission, which improves defective respiration, but does not rescue mtDNA depletion, cristae dysmorphology, or apoptotic sensitivity. Our data reveal that the multifaceted roles of OPA1 in mitochondria can be functionally uncoupled by modulating mitochondrial lipid metabolism, providing novel insights into the cellular relevance of mitochondrial fragmentation.
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