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DJ-1 deficiency impairs synaptic vesicle endocytosis and reavailability at nerve terminals

Authors
Kyung, JW | Kim, JM | Lee, W | Ha, TY  | Cha, SH | Chung, KH | Choi, DJ  | Jou, I  | Song, WK | Joe, EH  | Kim, SH | Park, SM
Citation
Proceedings of the National Academy of Sciences of the United States of America, 115(7). : 1629-1634, 2018
Journal Title
Proceedings of the National Academy of Sciences of the United States of America
ISSN
0027-84241091-6490
Abstract
Mutations in DJ-1 (PARK7) are a known cause of early-onset autosomal recessive Parkinson's disease (PD). Accumulating evidence indicates that abnormalities of synaptic vesicle trafficking underlie the pathophysiological mechanism of PD. In the present study, we explored whether DJ-1 is involved in CNS synaptic function. DJ-1 deficiency impaired synaptic vesicle endocytosis and reavailability without inducing structural alterations in synapses. Familial mutants of DJ-1 (M26I, E64D, and L166P) were unable to rescue defective endocytosis of synaptic vesicles, whereas WT DJ-1 expression completely restored endocytic function in DJ-1 KO neurons. The defective synaptic endocytosis shown in DJ-1 KO neurons may be attributable to alterations in membrane cholesterol level. Thus, DJ-1 appears essential for synaptic vesicle endocytosis and reavailability, and impairment of this function by familial mutants of DJ-1 may be related to the pathogenesis of PD.
Keywords
MeSH

DOI
10.1073/pnas.1708754115
PMID
29386384
Appears in Collections:
Journal Papers > Research Organization > Brain Disease Research Center
Journal Papers > Research Organization > Inflamm-aging Translational Research Center
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
Ajou Authors
박, 상면  |  조, 은혜  |  주, 일로  |  최, 동주  |  하, 태영
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