Amphiphysin is necessary for organization of the excitation–contraction coupling machinery of muscles, but not for synaptic vesicle endocytosis in Drosophila
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Amphiphysins 1 and 2 are enriched in the mammalian brain and are proposed to recruit dynamin to sites of endocytosis. Shorter amphiphysin 2 splice variants are also found ubiquitously, with an enrichment in skeletal muscle. At the Drosophila larval neuromuscular junction, amphiphysin is localized postsynaptically and amphiphysin mutants have no major defects in neurotransmission; they are also viable, but flightless. Like mammalian amphiphysin 2 in muscles,Drosophila amphiphysin does not bind clathrin, but can tubulate lipids and is localized on T-tubules.Amphiphysin mutants have a novel phenotype, a severely disorganized T-tubule/sarcoplasmic reticulum system. We therefore propose that muscle amphiphysin is not involved in clathrin-mediated endocytosis, but in the structural organization of the membrane-bound compartments of the excitation–contraction coupling machinery of muscles.
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Absence of the CLAP domain results in no detectable defects in synaptic vesicle endocytosis in Drosophila Amphiphysin mutant flies.
“Evidence from the analysis of Drosophila Amphiphysin, encoded by the unique Amphiphysin gene (and thought to be a BIN1 ortholog), show that absence of the CLAP domain results in no detectable defects in synaptic vesicle endocytosis in mutant flies [55–57].”
From Predominant expression of Alzheimer’s disease-associated BIN1 in mature oligodendrocytes and localization to white matter tracts (2016) · cites this paper as [56]
The section ‘Drosophila amphiphysin has no essential role in synaptic vesicle endocytosis’ reports that amphiphysin lacks clathrin-binding motifs and that mutants have little, if any, discernible defect in synaptic transmission. The paper does not identify a CLAP-domain deletion as the cause of that finding: it studied mutants lacking amphiphysin, not flies with a targeted deletion of that domain. Page numbers are unavailable in our copy. (LLM, conf=0.85)
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References 64 · Cited by 245
Research works printed but not linked: 6
- Crossley, A. 1978. Morphology and development of the Dro- sophila muscular system. In The genetics and biology of Drosophila, Vol. 2B (eds. M. Ashburner and T. Wright), pp. 499-560. Academic Press, San Francisco, CA.
- David, C., McPherson, P.S., Mundigl, O., and de Camilli, P. 1996. A role of amphiphysin in synaptic vesicle endocytosis suggested by its binding to dynamin in nerve terminals. Proc. Natl. Acad. Sci. 93: 331-335.
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- O'Kane, C.J. 1998. Enhancer traps. In Drosophila: A practical approach (ed. D.B. Roberts), pp. 131-178. Oxford University Press, Oxford, UK.
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- Authors
- Razzaq, A., Robinson, I. M., McMahon, H. T., Skepper, J. N., Su, Y., Zelhof, A. C., Jackson, A. P., Gay, N. J., & O'Kane, C. J.
- Affiliations
- Howard Hughes Medical Institute (US)
- ORCID
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2001-11-15
- Volume
- 15
- Issue
- 22
- Pages
- 2967-2979
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC312829
- OpenAlex
- W2149967863
- Cited by
- 245
- References
- 64
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 11 · 2023: 7 · 2022: 5 · 2021: 11 · 2020: 7 · 2019: 8 · 2018: 6 · 2017: 4 · 2016: 15 · 2015: 6 · 2014: 11 · 2013: 10 · 2012: 9
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust (039398/Z/93/Z, 052625)
- University of Cambridge
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Keywords
- amphiphysin, excitation-contraction coupling, T-tubules, sarcoplasmic reticulum, synaptic vesicle endocytosis, clathrin-mediated endocytosis, dynamin, neuromuscular junction, flightlessness, membrane tubulation
- MeSH terms
- Animals, Brain, Calcium, Clathrin, Drosophila, Electrophysiology, Endocytosis, Glutathione Transferase, Immunohistochemistry, Microscopy, Fluorescence, Models, Genetic, Muscles, Mutation, Nerve Tissue Proteins, Neuromuscular Junction, Phenotype, Protein Binding, Recombinant Fusion Proteins, Sarcoplasmic Reticulum, Tissue Distribution, Tubulin, Protein Structure, Tertiary, DNA, Complementary, Muscle, Skeletal, Microscopy, Confocal, Rats
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