Synapsins regulate α-synuclein functions

被引：71

作者：

Atias, Merav ^{[1
,2
]}

Tevet, Yaara ^{[1
,2
]}

Sun, Jichao ^{[3
]}

Stavsky, Alexandra ^{[1
,2
]}

Tal, Shani ^{[1
,2
]}

Kahn, Joy ^{[1
]}

Roy, Subhojit ^{[3
,4
]}

Gitler, Daniel ^{[1
,2
]}

机构：

[1] Ben Gurion Univ Negev, Dept Physiol & Cell Biol, Fac Hlth Sci, IL-84105 Beer Sheva, Israel

[2] Ben Gurion Univ Negev, Zlotowski Ctr Neurosci, IL-84105 Beer Sheva, Israel

[3] Univ Wisconsin, Dept Pathol & Lab Med, Madison, WI 53705 USA

[4] Univ Wisconsin, Dept Neurosci, Madison, WI 53705 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2019年 / 116卷 / 23期

基金：

以色列科学基金会;

关键词：

alpha synuclein; synapsin; neurotransmission; MICE LACKING; OVEREXPRESSION; MOBILITY; VESICLES; RELEASE;

D O I：

10.1073/pnas.1903054116

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

The normal function of alpha-synuclein (alpha-syn) remains elusive. Although recent studies suggest alpha-syn as a physiologic attenuator of synaptic vesicle (SV) recycling, mechanisms are unclear. Here, we show that synapsin-a cytosolic protein with known roles in SV mobilization and clustering-is required for presynaptic functions of alpha-syn. Our data offer a critical missing link and advocate a model where alpha-syn and synapsin cooperate to cluster SVs and attenuate recycling.

引用

页码：11116 / 11118

页数：3

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