Poliovirus Infection Transiently Increases COPII Vesicle Budding

被引:25
作者
Trahey, Meg [1 ,2 ]
Oh, Hyung Suk [3 ]
Cameron, Craig E. [3 ]
Hay, Jesse C. [1 ,2 ]
机构
[1] Univ Montana, Div Biol Sci, Missoula, MT 59812 USA
[2] Univ Montana, Ctr Struct & Funct Neurosci, Missoula, MT 59812 USA
[3] Penn State Univ, Dept Biochem & Mol Biol, University Pk, PA 16802 USA
基金
美国国家卫生研究院;
关键词
RETICULUM EXIT SITES; ENDOPLASMIC-RETICULUM; SECRETORY PATHWAY; SUBUNIT INTERACTIONS; PROTEIN SECRETION; SEC16; ER; REPLICATION; EXPORT; ORGANIZATION;
D O I
10.1128/JVI.01159-12
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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.
引用
收藏
页码:9675 / 9682
页数:8
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