Depletion of vesicle-tethering factor p115 causes mini-stacked Golgi fragments with delayed protein transport
Depletion of vesicle-tethering factor p115 causes mini-stacked Golgi fragments with delayed protein transport
复制标题
DOI：
10.1016/j.bbrc.2005.10.084
复制
发表时间：
2005-12-16
影响因子：
3.1
通讯作者：
Ikehara, Y
中科院分区：
文献类型：
--
作者：
Sohda, M;Misumi, Y;Ikehara, Y
耗尽p115与小干扰RNA引起的高尔基体的碎片，导致分散分布的堆叠短池和泡状结构（迷你堆叠高尔基体）。具有顺式和反式组织的小型堆叠高尔基体在蛋白质转运和糖基化中起作用，尽管在p115敲低细胞中分泌显著延迟。通过用breferdin A处理进一步破坏片段化的高尔基体，并通过去除药物重新组装成小型堆叠的高尔基体，如在对照细胞中观察到的。此外，p115基因敲除细胞保持从高尔基体到内质网的逆行运输，尽管该速率不如对照细胞有效。虽然在p115敲低的细胞中没有发现微管网络的改变，但破碎的高尔基体类似于用抗微管药物处理的细胞中的高尔基体。结果表明，p115参与囊泡运输内质网和高尔基体之间，沿着微管网络。(c)2005年爱思唯尔公司All rights reserved.
Depletion of p115 with small interfering RNA caused fragmentation of the Golgi apparatus, resulting in dispersed distribution of stacked short cisternae and a vesicular structure (mini-stacked Golgi). The mini-stacked Golgi with cis- and trans-organization is functional in protein transport and glycosylation, although secretion is considerably retarded in p] 15 knockdown cells. The fragmented Golgi was further disrupted by treatment with breferdin A and reassembled into the mini-stacked Golgi by removal of the drug, as observed in control cells. In addition, p115 knockdown cells maintained retrograde transport from the Golgi to the endoplasmic reticulum, although the rate was not as efficient as in control cells. While no alternation of microtubule networks was found in p115 knockdown cells, the fragmented Golgi resembled those in cells treated with anti-microtubule drugs. The results suggest that p115 is involved in vesicular transport between endoplasmic reticulum and the Golgi, along with microtubule networks. (c) 2005 Elsevier Inc. All rights reserved.