ArticleLife science alliance2020
Defective nucleotide-dependent assembly and membrane fusion in Mfn2 CMT2A variants improved by Bax.
Article in Life science alliance, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026Review
- Charcot-Marie-Tooth type 2A variants of mitofusin 2 sensitize cells to apoptotic cell death.Journal of cell science · 2025Article
- Molecular mechanisms of mitochondrial dynamics.Nature reviews. Molecular cell biology · 2025Review
- Mitochondrial hyperfusion induces metabolic remodeling in lung endothelial cells by modifying the activities of electron transport chain complexes I and III.Free radical biology & medicine · 2024Article
- A dominant negative mitofusin causes mitochondrial perinuclear clusters because of aberrant tethering.Life science alliance · 2023Article
- Mitochondria dysfunction in Charcot Marie Tooth 2B Peripheral Sensory Neuropathy.Communications biology · 2022Article
- Modulating mitofusins to control mitochondrial function and signaling.Nature communications · 2022Article
- The Role of Impaired Mitochondrial Dynamics in MFN2-Mediated Pathology.Frontiers in cell and developmental biology · 2022Review
- Characterization of a novel variant in the HR1 domain ofF1000Research · 2021Article
- Metabolic and biophysical study of the MFN2American journal of translational research · 2021Article
- Mitochondrial Surveillance by Cdc48/p97: MAD vs. Membrane Fusion.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mitofusins are members of the dynamin-related protein family of large GTPases that harness the energy from nucleotide hydrolysis to remodel membranes. Mitofusins possess four structural domains, including a GTPase domain, two extended helical bundles (HB1 and HB2), and a transmembrane region. We have characterized four Charcot-Marie-Tooth type 2A-associated variants with amino acid substitutions in Mfn2 that are proximal to the hinge that connects HB1 and HB2. A functional defect was not apparent in cells as the mitochondrial morphology of Mfn2-null cells was restored by expression of any of these variants. However, a significant fusion deficiency was observed in vitro, which was improved by the addition of crude cytosol extract or soluble Bax. All four variants had reduced nucleotide-dependent assembly in cis, but not trans, and this was also improved by the addition of Bax. Together, our data demonstrate an important role for this region in Mfn2 GTP-dependent oligomerization and membrane fusion and is consistent with a model where cytosolic factors such as Bax are masking molecular defects associated with Mfn2 disease variants in cells.
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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.