ArticleProceedings of the National Academy of Sciences of the United States of America2021
Evolutionarily related small viral fusogens hijack distinct but modular actin nucleation pathways to drive cell-cell fusion.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Pathogen-Mediated Cell Fusion and Actin Cytoskeleton.Advances in experimental medicine and biology · 2026Review
- Cell fusion in osteoclastogenesis.Biochemical Society transactions · 2025Review
- Multiple rotavirus species encode fusion-associated small transmembrane (FAST) proteins with cell type-specific activity.Journal of virology · 2025Article
- Cell surface crowding is a tunable energetic barrier to cell-cell fusion.Nature communications · 2025Article
- Intersectin1 promotes clathrin-mediated endocytosis by organizing and stabilizing endocytic protein interaction networks.Cell reports · 2024Article
- Avian deltacoronaviruses encode fusion-associated small transmembrane proteins that can induce syncytia formation.Virology · 2024Article
- Development and Characterization of an Oncolytic Human Adenovirus-Based Vector Co-Expressing the Adenovirus Death Protein and p14 Fusion-Associated Small Transmembrane Fusogenic Protein.International journal of molecular sciences · 2024Article
- Cell-cell fusion in cancer: The next cancer hallmark?The international journal of biochemistry & cell biology · 2024Review
- Virus-Induced Cell Fusion and Syncytia Formation.Results and problems in cell differentiation · 2024Article
- SARS-CoV-2 Syncytium under the Radar: Molecular Insights of the Spike-Induced Syncytia and Potential Strategies to Limit SARS-CoV-2 Replication.Journal of clinical medicine · 2023Review
- SARS-CoV-2 infection and viral fusogens cause neuronal and glial fusion that compromises neuronal activity.Science advances · 2023Article
- Eukaryotic fertilization and gamete fusion at a glance.Journal of cell science · 2022Article
- Plasma membrane protrusions mediate host cell-cell fusion induced byMolecular biology of the cell · 2022Article
- Determination of protoplast growth properties using quantitative single-cell tracking analysis.Plant methods · 2022Article
- Virus-Induced Membrane Fusion in Neurodegenerative Disorders.Frontiers in cellular and infection microbiology · 2022Review
- Article
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Fusion-associated small transmembrane (FAST) proteins are a diverse family of nonstructural viral proteins. Once expressed on the plasma membrane of infected cells, they drive fusion with neighboring cells, increasing viral spread and pathogenicity. Unlike viral fusogens with tall ectodomains that pull two membranes together through conformational changes, FAST proteins have short fusogenic ectodomains that cannot bridge the intermembrane gap between neighboring cells. One orthoreovirus FAST protein, p14, has been shown to hijack the actin cytoskeleton to drive cell-cell fusion, but the actin adaptor-binding motif identified in p14 is not found in any other FAST protein. Here, we report that an evolutionarily divergent FAST protein, p22 from aquareovirus, also hijacks the actin cytoskeleton but does so through different adaptor proteins, Intersectin-1 and Cdc42, that trigger N-WASP-mediated branched actin assembly. We show that despite using different pathways, the cytoplasmic tail of p22 can replace that of p14 to create a potent chimeric fusogen, suggesting they are modular and play similar functional roles. When we directly couple p22 with the parallel filament nucleator formin instead of the branched actin nucleation promoting factor N-WASP, its ability to drive fusion is maintained, suggesting that localized mechanical pressure on the plasma membrane coupled to a membrane-disruptive ectodomain is sufficient to drive cell-cell fusion. This work points to a common biophysical strategy used by FAST proteins to push rather than pull membranes together to drive fusion, one that may be harnessed by other short fusogens responsible for physiological cell-cell fusion.
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