Role of the influenza virus M1 protein in nuclear export of viral ribonucleoproteins
Role of the influenza virus M1 protein in nuclear export of viral ribonucleoproteins
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DOI：
10.1128/jvi.74.4.1781-1786.2000
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发表时间：
2000-02-01
影响因子：
5.4
通讯作者：
Whittaker, GR
中科院分区：
文献类型：
--
作者：
Bui, M;Wills, EG;Whittaker, GR
蛋白激酶抑制剂H7阻断流感病毒复制，抑制基质蛋白（M1）的产生，并导致病毒核糖核蛋白（vRNP）在感染后期滞留在细胞核中（K. Martin和A. Helenius，Cell 67：117-130，1991）。我们在这里表明，生产组装vRNP通常发生在H7处理的细胞，我们已经使用H7作为一种生化工具，以陷阱vRNP在细胞核中。当从细胞中去除H7时，在稳定表达重组M1的CHO细胞系中特异性诱导vRNP输出。类似地，表达来自Semliki森林病毒载体的重组M1的细胞的融合允许vRNP的核输出。然而，当细胞中存在H7时，输出没有被拯救，这意味着磷酸化在该过程中的额外作用。病毒NS 2蛋白在这些系统中检测不到。我们的结论是，流感病毒M1需要诱导vRNP核出口，但细胞磷酸化是一个额外的因素。
The protein kinase inhibitor H7 blocks influenza virus replication, inhibits production of the matrix protein (M1), and leads to a retention of the viral ribonucleoproteins (vRNPs) in the nucleus at late times of infection (K. Martin and A. Helenius, Cell 67:117-130, 1991). We show here that production of assembled vRNPs occurs normally in H7-treated cells, and we have used H7 as a biochemical tool to trap vRNPs in the nucleus. When H7 was removed from the cells, vRNP export was specifically induced in a CHO cell line stably expressing recombinant M1. Similarly, fusion of cells expressing recombinant M1 from a Semliki Forest virus vector allowed nuclear export of vRNPs, However, export was not rescued when H7 was present in the cells, implying an additional role for phosphorylation in this process. The viral NS2 protein was undetectable in these systems. We conclude that influenza virus M1 is required to induce vRNP nuclear export but that cellular phosphorylation is an additional factor.