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VPS35 dysfunction impairs lysosomal degradation of α-synuclein and exacerbates neurotoxicity in a Drosophila model of Parkinson's disease.

Abstract：

:Mutations in vacuolar protein sorting 35 (VPS35) have been linked to familial Parkinson's disease (PD). VPS35, a component of the retromer, mediates the retrograde transport of cargo from the endosome to the trans-Golgi network. Here we showed that retromer depletion increases the lysosomal turnover of the mannose 6-phosphate receptor, thereby affecting the trafficking of cathepsin D (CTSD), a lysosome protease involved in α-synuclein (αSYN) degradation. VPS35 knockdown perturbed the maturation step of CTSD in parallel with the accumulation of αSYN in the lysosomes. Furthermore, we found that the knockdown of Drosophila VPS35 not only induced the accumulation of the detergent-insoluble αSYN species in the brain but also exacerbated both locomotor impairments and mild compound eye disorganization and interommatidial bristle loss in flies expressing human αSYN. These findings indicate that the retromer may play a crucial role in αSYN degradation by modulating the maturation of CTSD and might thereby contribute to the pathogenesis of the disease.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Miura E,Hasegawa T,Konno M,Suzuki M,Sugeno N,Fujikake N,Geisler S,Tabuchi M,Oshima R,Kikuchi A,Baba T,Wada K,Nagai Y,Takeda A,Aoki M

doi

10.1016/j.nbd.2014.07.014

subject

Has Abstract

pub_date

2014-11-01 00:00:00

pages

1-13

eissn

0969-9961

issn

1095-953X

pii

S0969-9961(14)00215-0

journal_volume

71

pub_type

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