ArticleLife science alliance2019
Plasticity in salt bridge allows fusion-competent ubiquitylation of mitofusins and Cdc48 recognition.
Article in Life science alliance, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026Review
- A special latch in yeast mitofusin guarantees mitochondrial fusion by stabilizing self-assembly.Nature communications · 2025Article
- Charcot-Marie-Tooth type 2A variants of mitofusin 2 sensitize cells to apoptotic cell death.Journal of cell science · 2025Article
- E4 ubiquitin ligase promotes mitofusin turnover and mitochondrial stress response.Molecular cell · 2023Article
- Docking and stability defects in mitofusin highlight the proteasome as a potential therapeutic target.iScience · 2023Article
- A dominant negative mitofusin causes mitochondrial perinuclear clusters because of aberrant tethering.Life science alliance · 2023Article
- Dietary Supplements and Natural Products: An Update on Their Clinical Effectiveness and Molecular Mechanisms of Action During Accelerated Biological Aging.Frontiers in genetics · 2022Review
- Analysis of Protein Stability by Synthesis Shutoff.Bio-protocol · 2021Article
- Protein Quality Control at the Mitochondrial Surface.Frontiers in cell and developmental biology · 2021Review
- Mitochondrial Surveillance by Cdc48/p97: MAD vs. Membrane Fusion.International journal of molecular sciences · 2020Review
- Dual role of a GTPase conformational switch for membrane fusion by mitofusin ubiquitylation.Life science alliance · 2020Article
- Mitochondrial Quality Control Governed by Ubiquitin.Frontiers in cell and developmental biology · 2020Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitofusins are dynamin-related GTPases that drive mitochondrial fusion by sequential events of oligomerization and GTP hydrolysis, followed by their ubiquitylation. Here, we show that fusion requires a trilateral salt bridge at a hinge point of the yeast mitofusin Fzo1, alternatingly forming before and after GTP hydrolysis. Mutations causative of Charcot-Marie-Tooth disease massively map to this hinge point site, underlining the disease relevance of the trilateral salt bridge. A triple charge swap rescues the activity of Fzo1, emphasizing the close coordination of the hinge residues with GTP hydrolysis. Subsequently, ubiquitylation of Fzo1 allows the AAA-ATPase ubiquitin-chaperone Cdc48 to resolve Fzo1 clusters, releasing the dynamin for the next fusion round. Furthermore, cross-complementation within the oligomer unexpectedly revealed ubiquitylated but fusion-incompetent Fzo1 intermediates. However, Cdc48 did not affect the ubiquitylated but fusion-incompetent variants, indicating that Fzo1 ubiquitylation is only controlled after membrane merging. Together, we present an integrated model on how mitochondrial outer membranes fuse, a critical process for their respiratory function but also putatively relevant for therapeutic interventions.
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