Interaction of Stoned and Synaptotagmin in Synaptic Vesicle Endocytosis
| Autor: | Tim Fergestad, Kendal Broadie |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Dynamins
Vesicle fusion Adaptor Protein Complex 2 Neuromuscular Junction Presynaptic Terminals Nerve Tissue Proteins Pyridinium Compounds Biology Neurotransmission Synaptic Transmission Synaptic vesicle Exocytosis Synaptotagmin 1 GTP Phosphohydrolases Synaptotagmins chemistry.chemical_compound Adaptor Protein Complex alpha Subunits Animals Drosophila Proteins ARTICLE Neurotransmitter Fluorescent Dyes Dynamin Synaptic vesicle endocytosis Membrane Glycoproteins General Neuroscience Calcium-Binding Proteins Cell Membrane Synaptotagmin I Membrane Proteins HSP40 Heat-Shock Proteins Endocytosis Adaptor Protein Complex mu Subunits Cell biology Quaternary Ammonium Compounds Adaptor Proteins Vesicular Transport Phenotype chemistry Larva Mutation Potassium Drosophila Synaptic Vesicles Carrier Proteins Protein Binding |
| Zdroj: | The Journal of Neuroscience. 21:1218-1227 |
| ISSN: | 1529-2401 0270-6474 |
| DOI: | 10.1523/jneurosci.21-04-01218.2001 |
| Popis: | TheDrosophiladicistronicstonedlocus encodes two distinctive presynaptic proteins, Stoned A (STNA) and Stoned B (STNB); STNA is a novel protein without homology to known synaptic proteins, and STNB contains a domain with homology to the endocytotic protein AP50. Both Stoned proteins colocalize precisely with endocytotic proteins including the AP2 complex and Dynamin in the “lattice network” characteristic of endocytotic domains inDrosophilapresynaptic terminals. FM1–43 dye uptake studies instonedmutants demonstrate a striking decrease in the size of the endo–exo-cycling synaptic vesicle pool and loss of spatial regulation of the vesicular recycling intermediates. Mutant synapses display a significant delay in vesicular membrane retrieval after depolarization and neurotransmitter release. These studies suggest that the Stoned proteins play a role in mediating synaptic vesicle endocytosis. We have documented previously a highly specific synaptic mislocalization and degradation of Synaptotagmin I instonedmutants. Here we show that transgenic overexpression of Synaptotagmin I rescuesstonedembryonic lethality and restores endocytotic recycling to normal levels. Furthermore, overexpression of Synaptotagmin I in otherwise wild-type animals results in increased synaptic dye uptake, indicating that Synaptotagmin I directly regulates the endo–exo-cycling synaptic vesicle pool size. In parallel with recent biochemical studies, this genetic analysis strongly suggests that Stoned proteins regulate the AP2–Synaptotagmin I interaction during synaptic vesicle endocytosis. We conclude that Stoned proteins control synaptic transmission strength by mediating the retrieval of Synaptotagmin I from the plasma membrane. |
| Databáze: | OpenAIRE |
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