DJ-1 deficiency impairs synaptic vesicle endocytosis and reavailabilit…

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  • Writer 최고관리자
  • 2017-01-24


[BK21 Plus Seminar]
▶Subject: DJ-1 deficiency impairs synaptic vesicle endocytosis and reavailability at nerve terminals

▶Speaker: Sung Hyun Kim, Ph.D. (Department of Physiology, School of Medicine, Kyung Hee University)
▶Date: 4:30 PM/Feb. 2(Thu.)/2016
▶Place: Room 401, Chemistry Bldg.
Mutations in DJ-1 (PARK7) are a known cause for early-onset autosomal recessive Parkinson’s disease (PD). Growing evidence indicates that abnormalities of synaptic vesicle trafficking could be an important pathophysiological mechanism of PD. In the present study, we explored whether DJ-1 is involved in synaptic function at CNS synapses. We demonstrated that DJ-1 deficiency impairs synaptic vesicle endocytosis and synaptic vesicle reavailability without structural alterations of synapses or exocytosis. Expressions of familial mutants (M26I, E64D, and L166P) of DJ-1 are unable to rescue defective endocytosis of synaptic vesicles whereas WT DJ-1 expression completely restores the endocytic defect in DJ-1 KO neurons. In addition, DJ-1 deficiency reveals decreased levels of synaptojanin-1(synj1) expression, one of the key endocytic proteins, a mutation of which (R258Q) was recently identified in patients with Parkinsonism. Exogenously introducing WT synj1 in DJ-1 KO neurons partially rescues defective synaptic vesicle endocytosis. Moreover, overexpressing synj1 R258Q in DJ-1 KO neurons reveals a cumulative defect in synaptic vesicle endocytosis. Thus, DJ-1 is required for synaptic vesicle endocytosis and reavailability and functionally cooperates with synj1.

▶Inquiry: Prof. Prof. Lee, Seung-Jae(279-2351)
* This seminar will be given in English.
Please refrain from taking photos during seminars. *