Poliovirus infection transiently increases COPII vesicle budding.

Poliovirus infection transiently increases COPII vesicle budding.
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脊髓灰质炎病毒感染暂时增加 COPII 囊泡出芽。

DOI:
10.1128/jvi.01159-12
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发表时间:
2012
影响因子:
5.4
通讯作者:
Hay,JesseC
Hay,JesseC
中科院分区:
医学2区
文献类型:
--
作者:
Trahey,Meg;Oh,HyungSuk;Cameron,CraigE;Hay,JesseC

文献摘要

相似文献

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.