ArticleJournal of cell science2023
Myo19 tethers mitochondria to endoplasmic reticulum-associated actin to promote mitochondrial fission.
Article in Journal of cell science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 47 citations in OpenAlex.
- MSTO1 functions as a TRiC assembly factor linking cytosolic proteostasis to mitochondrial function.bioRxiv : the preprint server for biology · 2026Article
- An INF2-dependent actin-mediated step in inositol 1,4,5-trisphosphate receptor cluster formation and activity.Current biology : CB · 2026Article
- Mitochondrial Transport in Bone Metabolism Homeostasis: Molecular Mechanisms and Targeted Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Dynamic Proximity Networks of Myosin-19 (Myo19) and its Mitochondrial Receptors Miro2 and Metaxin-3.Molecular & cellular proteomics : MCP · 2026Article
- Non-muscle tropomyosins inhibit myosin-19 and dynamically localize to mitochondrially associated actin filaments.The Journal of biological chemistry · 2026Article
- Friction-driven scission: How nonlocal mechanisms contribute to membrane fission across domains of life.Science advances · 2026Review
- Macrophage Actin Cytoskeleton in Chronic Rejection.Results and problems in cell differentiation · 2026Review
- Targeting Mitochondria-Associated Endoplasmic Reticulum Membranes (MAMs): A Novel Therapeutic Strategy for Diabetic Complications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Crosstalk Between the Endoplasmic Reticulum and Mitochondria in Skeletal Muscle: Implications for Meat Quality.Animals : an open access journal from MDPI · 2025Review
- Article
- Structural-functional characterization of the MIRO1-TRAK1 complex.Nature communications · 2025Article
- Regulation of mitochondrial cristae organization by Myo19, Miro1 and Miro2, and metaxin 3.Journal of cell science · 2025Article
- Compositionally unique mitochondria in filopodia support cellular migration.Current biology : CB · 2025Article
- A novel, rapidly progressive ataxia due to a spontaneous Myo5a mutation in mice impairs transport proteins and alters mitochondria.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Molecular mechanisms of mitochondrial dynamics.Nature reviews. Molecular cell biology · 2025Review
- Mitochondria- and ER-associated actin are required for mitochondrial fusion.Nature communications · 2025Article
- MYO19 is associated with tumor progression, immune evasion, ferroptosis-related signatures in lung squamous cell carcinoma.Frontiers in oncology · 2025Article
- Mitochondrial membrane synthesis, remodelling and cellular trafficking.Journal of inherited metabolic disease · 2025Review
- Revealing mitochondrial architecture and functions with single molecule localization microscopy.Biology of the cell · 2025Review
- Mitochondrial dynamics at the intersection of macrophage polarization and metabolism.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondrial homeostasis requires a dynamic balance of fission and fusion. The actin cytoskeleton promotes fission, and we found that the mitochondrially localized myosin, myosin 19 (Myo19), is integral to this process. Myo19 knockdown induced mitochondrial elongation, whereas Myo19 overexpression induced fragmentation. This mitochondrial fragmentation was blocked by a Myo19 mutation predicted to inhibit ATPase activity and strong actin binding but not by mutations predicted to affect the working stroke of the motor that preserve ATPase activity. Super-resolution imaging indicated a dispersed localization of Myo19 on mitochondria, which we found to be dependent on metaxins. These observations suggest that Myo19 acts as a dynamic actin-binding tether that facilitates mitochondrial fragmentation. Myo19-driven fragmentation was blocked by depletion of either the CAAX splice variant of the endoplasmic reticulum (ER)-anchored formin INF2 or the mitochondrially localized F-actin nucleator Spire1C (a splice variant of Spire1), which together polymerize actin at sites of mitochondria-ER contact for fission. These observations imply that Myo19 promotes fission by stabilizing mitochondria-ER contacts; we used a split-luciferase system to demonstrate a reduction in these contacts following Myo19 depletion. Our data support a model in which Myo19 tethers mitochondria to ER-associated actin to promote mitochondrial fission.
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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.