EIF3i affects vesicular stomatitis virus growth by interacting with matrix protein.
EIF3i affects vesicular stomatitis virus growth by interacting with matrix protein.
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EIF3i 通过与基质蛋白相互作用影响水泡性口炎病毒生长
DOI：
10.1016/j.vetmic.2017.10.021
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发表时间：
2017-12
影响因子：
3.3
通讯作者：
Zhao K
中科院分区：
文献类型：
--
作者：
Pan W;Song D;He W;Lu H;Lan Y;Li H;Gao F;Zhao K
VSV M蛋白与eIF 3的i亚基相互作用。与eIF 3 i相互作用的M区域位于122至181个氨基酸内。M-eIF 3 i相互作用影响VSV生长。水泡性口炎病毒（VSV）的基质蛋白在病毒基因组复制和病毒体产生期间执行多种功能，并且参与调节有利于病毒复制的多种宿主信号传导途径。为了在受感染的细胞内执行许多功能，M蛋白需要招募细胞伴侣。为了更好地了解M在VSV复制过程中的作用，我们使用双杂交系统寻找相互作用的伙伴。真核生物翻译起始因子3，亚基i（eIF 3 i）被确定为M-结合伴侣，并通过GST下拉和激光共聚焦分析验证了这种相互作用。通过诱变分析，我们发现氨基酸122和181之间的M的一些突变体削弱但没有完全消除M-eIF 3 i相互作用。此外，通过RNA干扰敲低eIF 3 i在早期阶段降低了病毒复制和转录，但在后期阶段导致增加。VSV转录在感染后4 h增加，但在感染后8和12 h后，eIF 3 i的过表达后没有改变。最后，我们还证明了VSV可以抑制Akt 1的活性，并且eIF 3 i的敲低抑制了由磷酸化Akt 1调节的ISGs的表达。这些结果表明eIF 3 i可能通过调节宿主在HeLa细胞中的抗病毒反应来影响VSV的生长。
VSV M protein interacts with the i subunit of eIF3. The region of M that interacts with eIF3i is located within the 122- to -181 amino acids. M–eIF3i interaction affects VSV growth. The matrix protein of vesicular stomatitis virus (VSV) performs multiple functions during viral genome replication and virion production and is involved in modulating multiple host signaling pathways that favor virus replication. To perform numerous functions within infected cells, the M protein needs to recruit cellular partners. To better understand the role of M during VSV replication, we looked for interacting partners by using the two-hybrid system. The eukaryotic translation initiation factor 3, subunit i (eIF3i) was identified to be an M-binding partner, and this interaction was validated by GST pull-down and laser confocal assays. Through a mutagenesis analysis, we found that some mutants of M between amino acids 122 and 181 impaired but did not completely abolish the M–eIF3i interaction. Furthermore, the knockdown of eIF3i by RNA interference decreased viral replication and transcription in the early stages but led to increase in later stages. VSV transcription was increased at 4 h post-infection but was not changed at 8 and 12 h post-infection after the over-expression of eIF3i. Finally, we also demonstrated that VSV could inhibit the activity of Akt1 and that the knockdown of eIF3i inhibited the expression of the ISGs regulated by phospho-Akt1. These results indicated that eIF3i may affect VSV growth by regulating the host antiviral response in HeLa cells.
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影响因子：
5.4
作者：
Raux, Helene;Obiang, Linda;Gaudin, Yves
通讯作者：
Gaudin, Yves
影响因子：
3.7
作者：
GAUDIN, Y;BARGE, A;RUIGROK, RWH
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RUIGROK, RWH
影响因子：
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作者：
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Lyles, DS
影响因子：
5.4
作者：
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通讯作者：
Schnell, MJ
影响因子：
5.4
作者：
Kopecky, SA;Willingham, MC;Lyles, DS
通讯作者：
Lyles, DS