ArticleThe Journal of cell biology2023
Human atlastin-3 is a constitutive ER membrane fusion catalyst.
Article in The Journal of cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 9 citations in OpenAlex.
- Atlastin-2-mediated endoplasmic reticulum membrane tethering is critical for flavivirus replication.PLoS biology · 2026Article
- Rab10 Promotes Atlastin-Mediated Endoplasmic Reticulum Membrane Fusion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- ATL2 Recruits TRAK1 to Promote Mitochondrial Transport at ER-Mitochondria Contact Sites.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Connecting tubules: mechanisms of endoplasmic reticulum membrane fusion.Biochemical Society transactions · 2025Review
- Connecting tubules: mechanisms of endoplasmic reticulum membrane fusion.Biochemical Society transactions · 2025Review
- Structural and functional characterization of the brain-specific dynamin superfamily member RNF112.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- Network-based modelling reveals cell-type enriched patterns of non-coding RNA regulation during human skeletal muscle remodelling.bioRxiv : the preprint server for biology · 2024Article
- Network-based modelling reveals cell-type enriched patterns of non-coding RNA regulation during human skeletal muscle remodelling.NAR molecular medicine · 2024Article
- Dissecting the mechanism of atlastin-mediated homotypic membrane fusion at the single-molecule level.Nature communications · 2024Article
- Yeast lunapark regulates the formation ofiScience · 2023Article
- The atlastin ER morphogenic proteins promote formation of a membrane penetration site during non-enveloped virus entry.Journal of virology · 2023Article
- The atlastin paralogs: The complexity in the tails.The Journal of cell biology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Homotypic membrane fusion catalyzed by the atlastin (ATL) GTPase sustains the branched endoplasmic reticulum (ER) network in metazoans. Our recent discovery that two of the three human ATL paralogs (ATL1/2) are C-terminally autoinhibited implied that relief of autoinhibition would be integral to the ATL fusion mechanism. An alternative hypothesis is that the third paralog ATL3 promotes constitutive ER fusion with relief of ATL1/2 autoinhibition used conditionally. However, published studies suggest ATL3 is a weak fusogen at best. Contrary to expectations, we demonstrate here that purified human ATL3 catalyzes efficient membrane fusion in vitro and is sufficient to sustain the ER network in triple knockout cells. Strikingly, ATL3 lacks any detectable C-terminal autoinhibition, like the invertebrate Drosophila ATL ortholog. Phylogenetic analysis of ATL C-termini indicates that C-terminal autoinhibition is a recent evolutionary innovation. We suggest that ATL3 is a constitutive ER fusion catalyst and that ATL1/2 autoinhibition likely evolved in vertebrates as a means of upregulating ER fusion activity on demand.
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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.