Sohda Miwa, Misumi Yoshio, Yoshimura Shin-ichiro, Nakamura Nobuhiro, Fusano Takami, Sakisaka Shotaro, Ogata Shigenori, Fujimoto Junichro, Kiyokawa Nobutaka, Ikehara Yukio
Department of Cell Biology, Fukuoka University School of Medicine, Jonan-ku, Fukuoka 814-0180, Japan.
Biochem Biophys Res Commun. 2005 Dec 16;338(2):1268-74. doi: 10.1016/j.bbrc.2005.10.084. Epub 2005 Oct 24.
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 p115 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.
用小干扰RNA耗尽p115会导致高尔基体碎片化，导致堆叠的短扁平囊泡和囊泡结构（微型堆叠高尔基体）分散分布。具有顺式和反式组织的微型堆叠高尔基体在蛋白质运输和糖基化方面具有功能，尽管在p115敲低细胞中分泌明显延迟。如在对照细胞中观察到的那样，碎片化的高尔基体在用布雷菲德菌素A处理后进一步被破坏，并通过去除药物重新组装成微型堆叠高尔基体。此外，p115敲低细胞维持从高尔基体到内质网的逆行运输，尽管其速率不如对照细胞有效。虽然在p115敲低细胞中未发现微管网络的改变，但碎片化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与微管网络一起参与内质网和高尔基体之间的囊泡运输。
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