Retrograde transport of TrkB-containing autophagosomes via the adaptor AP-2 mediates neuronal complexity and prevents neurodegeneration

Natalia L. Kononenko (), Gala A. Claßen, Marijn Kuijpers, Dmytro Puchkov, Tanja Maritzen, Aleksandra Tempes, Anna R. Malik, Agnieszka Skalecka, Sujoy Bera, Jacek Jaworski and Volker Haucke ()
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Natalia L. Kononenko: Leibniz-Institut für Molekulare Pharmakologie
Gala A. Claßen: Leibniz-Institut für Molekulare Pharmakologie
Marijn Kuijpers: Leibniz-Institut für Molekulare Pharmakologie
Dmytro Puchkov: Leibniz-Institut für Molekulare Pharmakologie
Tanja Maritzen: Leibniz-Institut für Molekulare Pharmakologie
Aleksandra Tempes: Laboratory of Molecular and Cellular Neurobiology, International Institute of Molecular and Cell Biology
Anna R. Malik: Laboratory of Molecular and Cellular Neurobiology, International Institute of Molecular and Cell Biology
Agnieszka Skalecka: Laboratory of Molecular and Cellular Neurobiology, International Institute of Molecular and Cell Biology
Sujoy Bera: CECAD Research Center, University of Cologne
Jacek Jaworski: Laboratory of Molecular and Cellular Neurobiology, International Institute of Molecular and Cell Biology
Volker Haucke: Leibniz-Institut für Molekulare Pharmakologie

Nature Communications, 2017, vol. 8, issue 1, 1-16

Abstract: Abstract 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.

Date: 2017
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DOI: 10.1038/ncomms14819

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