Sindbis virus usurps the cellular HuR protein to stabilize its transcripts and promote productive infections in mammalian and mosquito cells.
Sindbis virus usurps the cellular HuR protein to stabilize its transcripts and promote productive infections in mammalian and mosquito cells.
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DOI：
10.1016/j.chom.2010.07.003
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发表时间：
2010-08-19
影响因子：
30.3
通讯作者：
Wilusz J
中科院分区：
文献类型：
--
作者：
Sokoloski KJ;Dickson AM;Chaskey EL;Garneau NL;Wilusz CJ;Wilusz J
病毒保护其转录物免受细胞RNA衰变机制影响的机制以及这种保护的生物学相关性在很大程度上是未知的。我们证明辛德毕斯病毒在其RNA中使用富含U的3' UTR序列来在人类和蚊子细胞的感染期间招募细胞HuR蛋白。HuR以高特异性和亲和力结合病毒RNA。此外，辛德毕斯病毒在感染期间诱导HuR蛋白选择性移出哺乳动物细胞的细胞核，从而增加病毒可用的蛋白质的细胞质库。最后，HuR的敲低导致辛德毕斯病毒RNA的衰变速率显著增加，并减少人和蚊子细胞中的病毒产量。总的来说，这些数据表明辛德毕斯病毒和可能的其他甲病毒，篡夺HuR蛋白，以避免细胞mRNA衰变机制，并保持高生产性感染。
The mechanisms utilized by viruses to protect their transcripts from the cellular RNA decay machinery, as well as the biological relevance of this protection, are largely unknown. We demonstrate that Sindbis virus uses U-rich 3’ UTR sequences in its RNAs to recruit the cellular HuR protein during infections of both human and mosquito cells. HuR binds viral RNAs with high specificity and affinity. Furthermore, Sindbis virus induces the selective movement of HuR protein out of the nucleus of mammalian cells during infection thereby increasing the cytoplasmic pool of the protein available to the virus. Finally, knockdown of HuR results in a significant increase in the rate of decay of Sindbis virus RNAs and diminishes viral yields in both human and mosquito cells. Collectively these data indicate that Sindbis virus, and likely other alphaviruses, usurp the HuR protein to avoid the cellular mRNA decay machinery and maintain a highly productive infection.
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