ArticleThe Journal of cell biology2022
Reconstitution of human atlastin fusion activity reveals autoinhibition by the C terminus.
Article in The Journal of cell biology, 2022. 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, 16 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
- 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
- Dissecting the mechanism of atlastin-mediated homotypic membrane fusion at the single-molecule level.Nature communications · 2024Article
- Allosteric control of dynamin-related protein 1 through a disordered C-terminal Short Linear Motif.Nature communications · 2024Article
- Article
- The atlastin paralogs: The complexity in the tails.The Journal of cell biology · 2023Article
- Human atlastin-3 is a constitutive ER membrane fusion catalyst.The Journal of cell biology · 2023Article
- Human atlastins are sufficient to drive the fusion of liposomes with a physiological lipid composition.The Journal of cell biology · 2023Article
- Membrane fusion byMolecular biology of the cell · 2022Article
- A role for endoplasmic reticulum dynamics in the cellular distribution of microtubules.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
ER network formation depends on membrane fusion by the atlastin (ATL) GTPase. In humans, three paralogs are differentially expressed with divergent N- and C-terminal extensions, but their respective roles remain unknown. This is partly because, unlike Drosophila ATL, the fusion activity of human ATLs has not been reconstituted. Here, we report successful reconstitution of fusion activity by the human ATLs. Unexpectedly, the major splice isoforms of ATL1 and ATL2 are each autoinhibited, albeit to differing degrees. For the more strongly inhibited ATL2, autoinhibition mapped to a C-terminal α-helix is predicted to be continuous with an amphipathic helix required for fusion. Charge reversal of residues in the inhibitory domain strongly activated its fusion activity, and overexpression of this disinhibited version caused ER collapse. Neurons express an ATL2 splice isoform whose sequence differs in the inhibitory domain, and this form showed full fusion activity. These findings reveal autoinhibition and alternate splicing as regulators of atlastin-mediated ER fusion.
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