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The transport mechanism of transport vesicle on membrane traffic from endoplasmic reticulum to the Golgi apparatus

转运囊泡对内质网至高尔基体膜运输的转运机制

基本信息

批准号：
17570122
负责人：
MIWA Sohda
金额：
$ 2.24万
依托单位：
Fukuoka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2006
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-17570122/
关键词：
Golgi apparatus VTCs 小胞輸送小胞体微小管

项目摘要

Membrane and secretion proteins synthesized on ER are transported first to the Golgi apparatus. After the maturation of the sugar chain modification etc. there, proteins are sorted and transported into each localization compartment. Recently, the mechanism of the transport from ER to Golgi has been becoming clear a little. The mechanism of the transport from ER to Golgi has become clear to some degree. Recently, it is thought that the COPII vesicles budding from ER exit sites that lie scattered in the cell periphery fuse each other to form bigger membrane structure VTCs (tubulo vesicular compartments), and then VTCs are carried to the Golgi apparatus around nuclear.I have analyzed the function of vesicle tethering factor p115 using p115 knock down (KD) cells. By the process of the analysis, p115 has been found playing important role to transport the membrane structure that budding as COPII vesicles to the Golgi apparatus. Depletion of p115 caused fragmentation of the Golgi apparatus. The fragmented Golgi was distinct from VTCs and ER exit sites, maintained mini-stack structures with cis-to trans-organization. While no alternation of microtubule networks was found in p115 KD cells, the fragmented Golgi resembled those in cells treated with anti-microtubule drug. Furthermore, p115 was co-precipitated with anti Bicaudal-D antibody. Bicaudal-D is known to interact with microtubule motor, dynein-dynactin complex. These results suggested that the scattered Golgi in p115 KD cells was derived from VTCs, which were not able to interact with the motor complex on microtubules, resulting in the formation of the mini-stacked Golgi distributed near the ER exit sites. It is likely t hat p115 plays a role in promoting the interaction of COPII-derived VTCs with the motor complex on microtubules.

在内质网上合成的膜和分泌蛋白首先被运送到高尔基体。在那里的糖链修饰等成熟后，蛋白质被分类并转运到每个定位室中。近年来，人们对内质网向高尔基体的转运机制有了一些了解。从内质网到高尔基体的转运机制已经在一定程度上清楚了。最近，人们认为分散在细胞外围的内质网出口出芽的COPII囊泡相互融合形成更大的膜结构VTCs（管状囊泡室），然后VTCs被携带到核周围的高尔基体。我用p115敲低（KD）细胞分析了囊泡系栓因子p115的功能。在分析过程中发现p115在将以COPII囊泡出芽的膜结构转运到高尔基体中起重要作用。p115的耗竭导致高尔基体碎裂。碎片化的高尔基体不同于VTCs和ER出口点，保持着从顺向到跨组织的小堆栈结构。虽然在p115 KD细胞中没有发现微管网络的改变，但碎片化的高尔基体与抗微管药物处理的细胞相似。此外，p115与抗Bicaudal-D抗体共沉淀。Bicaudal-D已知与微管马达，动力蛋白复合物相互作用。这些结果表明p115 KD细胞中分散的高尔基体来源于VTCs， VTCs不能与微管上的运动复合物相互作用，导致分布在内质网出口附近的微堆叠高尔基体形成。p115可能在促进copii衍生的VTCs与微管上的运动复合物的相互作用中起作用。

项目成果

期刊论文数量（6）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

The interaction of two tethering factors, p115 and COG complex, is required for Golgi integrity

DOI：
10.1111/j.1600-0854.2006.00530.x
发表时间：
2007-03-01
期刊：
TRAFFIC
影响因子：
4.5
作者：
Sohda, Miwa;Misumi, Yoshio;Ikehara, Yukio
通讯作者：
Ikehara, Yukio

Depletion of vesicle-tethering factor pll5 causes mini-stacked Golgi fragments with delayed protein transport.

囊泡束缚因子 pll5 的耗竭会导致高尔基体碎片迷你堆积，并导致蛋白质转运延迟。

DOI：
发表时间：
2005
期刊：
Biochem. Biophys. Res. Commun 338・2
影响因子：
0
作者：
M.Sohda;Y.Misumi;S.Yoshimura;N.Nakamura;T.Fusano;S.Sakisaka;S.Ogata;J.Fujimoto;N.Kiyokawa;Y.Ikehara.
通讯作者：
Y.Ikehara.

Depletion of vesicle-tethering factor p115 causes mini-stacked Golgi fragments with delayed protein transport