AP180 Couples Protein Retrieval to Clathrin‐Mediated Endocytosis of Synaptic Vesicles

摘要: How clathrin-mediated endocytosis (CME) retrieves vesicle proteins into newly formed synaptic vesicles (SVs) remains a major puzzle. Besides its roles in stimulating clathrin-coated formation and regulating SV size, the clathrin assembly protein AP180 has been identified as key player retrieving proteins. The mechanisms by which recruits are not fully understood. Here, we show that following acute inactivation of Drosophila, recycling is severely impaired at larval neuromuscular synapse based on analyses FM 1-43 uptake ultrastructure. More dramatically, activity important to maintain integrity complexes plasma membrane during endocytosis. These observations suggest normally clusters together recycling. Consistent with this notion, composition distribution altered mutant flies. Finally, co-immunoprecipitates proteins, including vesicular glutamate transporter neuronal synaptobrevin. results reveal new mode couples retrieval CME SVs. also genetically linked Alzheimer's disease. Hence, findings study may provide mechanistic insight role dysfunction