Cooper M, Goodwin D J, Hall K T, Stevenson A J, Meredith D M, Markham A F, Whitehouse A
J Gen Virol. 1999 May;80 ( Pt 5):1311-1316. doi: 10.1099/0022-1317-80-5-1311.
The herpesvirus saimiri (HVS) gene product encoded by ORF 57 shares limited C-terminal similarity with herpes simplex virus 1 ICP27, a protein that has been demonstrated to be involved in the inhibition of host-cell splicing and is responsible for the redistribution of components of the spliceosome. It has previously been shown that ORF 57 can either activate or repress viral gene expression by a post-transcriptional mechanism. Furthermore, repression of gene expression by ORF 57 is dependent on the presence of an intron within the target gene coding region. In this report, it is shown that HVS infection results in the redistribution of the SC-35 splicing factor in the infected cell nucleus. Furthermore, the redistributed SC-35 colocalized with the ORF 57 protein product and expression of the protein alone was sufficient to cause the redistribution of the spliceosome components. These results suggest that the mechanism by which ORF 57 down-regulates expression of intron-containing genes involves the redistribution of the spliceosome complex.
由开放阅读框57（ORF 57）编码的猴疱疹病毒（HVS）基因产物与单纯疱疹病毒1型的ICP27在C端具有有限的相似性，ICP27蛋白已被证明参与抑制宿主细胞剪接，并负责剪接体组分的重新分布。此前已有研究表明，ORF 57可通过转录后机制激活或抑制病毒基因表达。此外，ORF 57对基因表达的抑制取决于靶基因编码区内内含子的存在。在本报告中，研究表明HVS感染导致感染细胞核内SC-35剪接因子的重新分布。此外，重新分布的SC-35与ORF 57蛋白产物共定位，单独表达该蛋白就足以导致剪接体组分的重新分布。这些结果表明，ORF 57下调含内含子基因表达的机制涉及剪接体复合物的重新分布。
