期刊
NATURE COMMUNICATIONS
卷 8, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms14819
关键词
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资金
- German Research Foundation [SFB958/A01]
- NeuroCure Cluster of Excellence [Exc-257]
- Reinhart-Koselleck Award
- NeuroCure Female PostDoc fellowship
- Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) [Exc 229]
- National Science Centre [2011/03/B/NZ3/01970]
- Foundation for Polish Science 'Mistrz' Professorial Subsidy and Fellowship
- H2020 EU Marie Curie IF fellowship
Autophagosomes primarily mediate turnover of cytoplasmic proteins or organelles to provide nutrients and eliminate damaged proteins. In neurons, autophagosomes form in distal axons and are trafficked retrogradely to fuse with lysosomes in the soma. Although defective neuronal autophagy is associated with neurodegeneration, the function of neuronal autophagosomes remains incompletely understood. We show that in neurons, autophagosomes promote neuronal complexity and prevent neurodegeneration in vivo via retrograde transport of brain-derived neurotrophic factor (BDNF)-activated TrkB receptors. p150Glued/dynactin-dependent transport of TrkB-containing autophagosomes requires their association with the endocytic adaptor AP-2, an essential protein complex previously thought to function exclusively in clathrin-mediated endocytosis. These data highlight a novel non-canonical function of AP-2 in retrograde transport of BDNF/TrkB-containing autophagosomes in neurons and reveal a causative link between autophagy and BDNF/TrkB signalling.
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