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脊髓灰质炎病毒感染会短暂增加 COPII 囊泡出芽。

Poliovirus infection transiently increases COPII vesicle budding.

机构信息

Division of Biological Sciences and Center for Structural and Functional Neuroscience, The University of Montana, Missoula, Montana, USA.

出版信息

J Virol. 2012 Sep;86(18):9675-82. doi: 10.1128/JVI.01159-12. Epub 2012 Jun 27.

Abstract

Poliovirus (PV) requires membranes of the host cell's secretory pathway to generate replication complexes (RCs) for viral RNA synthesis. Recent work identified the intermediate compartment and the Golgi apparatus as the precursors of the replication "organelles" of PV (N. Y. Hsu et al., Cell 141:799-811, 2010). In this study, we examined the effect of PV on COPII vesicles, the secretory cargo carriers that bud from the endoplasmic reticulum and homotypically fuse to form the intermediate compartment that matures into the Golgi apparatus. We found that infection by PV results in a biphasic change in functional COPII vesicle biogenesis in cells, with an early enhancement and subsequent inhibition. Concomitant with the early increase in COPII vesicle formation, we found an increase in the membrane fraction of Sec16A, a key regulator of COPII vesicle formation. We suggest that the early burst in COPII vesicle formation detected benefits PV by increasing the precursor pool required for the formation of its RCs.

摘要

脊髓灰质炎病毒(PV)需要利用宿主细胞分泌途径的膜来生成用于病毒 RNA 合成的复制复合物(RC)。最近的研究工作确定了中间隔室和高尔基体是 PV 复制“细胞器”的前体(N. Y. Hsu 等人,《细胞》141:799-811,2010)。在这项研究中,我们研究了 PV 对 COPII 囊泡的影响,COPII 囊泡是从内质网出芽并同源融合形成中间隔室,进而成熟为高尔基体的分泌货物载体。我们发现,PV 感染会导致细胞中功能性 COPII 囊泡生物发生发生双峰变化,早期增强,随后抑制。与 COPII 囊泡形成的早期增加同时,我们发现 Sec16A 的膜部分增加,Sec16A 是 COPII 囊泡形成的关键调节因子。我们认为,早期检测到的 COPII 囊泡形成的爆发有利于 PV,因为它增加了形成其 RC 所需的前体池。

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