EndophilinA-dependent coupling between activity-induced calcium influx and synaptic autophagy is disrupted by a Parkinson-risk mutation

• Published in: Neuron (Cambridge, Mass.) Vol. 111; no. 9; pp. 1402 - 1422.e13
• Main Authors: Bademosi, Adekunle T., Decet, Marianna, Kuenen, Sabine, Calatayud, Carles, Swerts, Jef, Gallego, Sandra F., Schoovaerts, Nils, Karamanou, Spyridoula, Louros, Nikolaos, Martin, Ella, Sibarita, Jean-Baptiste, Vints, Katlijn, Gounko, Natalia V., Meunier, Frédéric A., Economou, Anastassios, Versées, Wim, Rousseau, Frederic, Schymkowitz, Joost, Soukup, Sandra-F., Verstreken, Patrik
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 03.05.2023; Cell Press
• Subjects: Animals; Autophagy - genetics; Ca2+ influx; Calcium - metabolism; Dopaminergic Neurons - metabolism; Drosophila - metabolism; endophilinA; Humans; Mutation - genetics; neuronal activity; Parkinson disease; Parkinson Disease - genetics; Parkinson Disease - metabolism; synaptic autophagy; Parkinson disease; synaptic autophagy; neuronal activity; Ca2+ influx; endophilinA; Ca(2+) influx

Neuronal activity causes use-dependent decline in protein function. However, it is unclear how this is coupled to local quality control mechanisms. We show in Drosophila that the endocytic protein Endophilin-A (EndoA) connects activity-induced calcium influx to synaptic autophagy and neuronal surviv...