ArticleLife science alliance2023
A dominant negative mitofusin causes mitochondrial perinuclear clusters because of aberrant tethering.
Article in Life science alliance, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Spatial control of mitochondrial retrograde signaling by nuclear pore-associated contact sites.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial Dynamics Disorder Drives Nucleus Pulposus Cell Senescence in Lumbar Scoliosis of Aging Bipedal Rats Under Asymmetric Force.Stem cells international · 2026Article
- Modulating inter-mitochondrial contacts to increase membrane potential for mitigating blue light damage.bioRxiv : the preprint server for biology · 2025Article
- Structural insights into GTP-coupled conformational changes in Mfn1 revealed by time-resolved transition metal ion FRET.bioRxiv : the preprint server for biology · 2025Article
- Charcot-Marie-Tooth type 2A variants of mitofusin 2 sensitize cells to apoptotic cell death.Journal of cell science · 2025Article
- Activating AMPK improves pathological phenotypes due to mtDNA depletion.The FEBS journal · 2025Article
- Knockdown ofCells · 2025Article
- Complex interplay between RAS GTPases and RASSF effectors regulates subcellular localization of YAP.EMBO reports · 2024Article
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Authors and funding
2 authors.
Funding
Abstract
In vertebrates, mitochondrial outer membrane fusion is mediated by two mitofusin paralogs, Mfn1 and Mfn2, conserved dynamin superfamily proteins. Here, we characterize a variant of mitofusin reported in patients with CMT2A where a serine is replaced with a proline (Mfn2-S350P and the equivalent in Mfn1, S329P). This serine is in a hinge domain (Hinge 2) that connects the globular GTPase domain to the adjacent extended helical bundle. We find that expression of this variant results in prolific and stable mitochondrial tethering that also blocks mitochondrial fusion by endogenous wild-type mitofusin. The formation of mitochondrial perinuclear clusters by this CMT2A variant requires normal GTPase domain function and formation of a mitofusin complex across two membranes. We propose that conformational dynamics mediated by Hinge 2 and regulated by GTP hydrolysis are disrupted by the substitution of proline at S329/S350 and this prevents progression from tethering to membrane fusion. Thus, our data are consistent with a model for mitofusin-mediated membrane fusion where Hinge 2 supports a power stroke to progress from the tethering complex to membrane fusion.
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