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人巨细胞病毒的UL69反式激活蛋白与DEXD/H盒RNA解旋酶UAP56相互作用,以促进未剪接RNA的细胞质积累。

The UL69 transactivator protein of human cytomegalovirus interacts with DEXD/H-Box RNA helicase UAP56 to promote cytoplasmic accumulation of unspliced RNA.

作者信息

Lischka Peter, Toth Zsolt, Thomas Marco, Mueller Regina, Stamminger Thomas

机构信息

Institut für Klinische und Molekulare Virologie, Universität Erlangen-Nürnberg, Schlossgarten 4, 91054 Erlangen, Germany.

出版信息

Mol Cell Biol. 2006 Mar;26(5):1631-43. doi: 10.1128/MCB.26.5.1631-1643.2006.

Abstract

The UL69 gene product of human cytomegalovirus belongs to a family of regulatory proteins conserved among all herpesviruses that have in part been characterized as posttranscriptional transactivators participating in the nuclear export of RNA. Recent experiments suggested that pUL69 also acts as a posttranscriptional activator since it was demonstrated that nucleocytoplasmic shuttling via a CRM1-independent nuclear export signal is a prerequisite for its stimulatory effect on gene expression. Based on these findings we initiated studies to investigate the role of pUL69 in mRNA export and demonstrate that pUL69 efficiently promotes the cytoplasmic accumulation of unspliced RNA. Furthermore, we show that this pUL69 activity is linked to the cellular mRNA export machinery by direct protein interaction with the highly related DEXD/H-box RNA helicases UAP56 and URH49. Particularly, we identified a 12-amino-acid domain within the N terminus of pUL69 which is required for binding to UAP56 and URH49, and we could demonstrate that UAP56 interaction and nucleocytoplasmic shuttling are both prerequisites for pUL69-mediated mRNA export. Thus, we identified a novel cellular target which provides a herpesviral regulatory protein with access to a conserved cellular transport system in order to promote nuclear export of unspliced RNA.

摘要

人巨细胞病毒的UL69基因产物属于在所有疱疹病毒中保守的一类调节蛋白,这类蛋白部分已被表征为参与RNA核输出的转录后反式激活因子。最近的实验表明,pUL69也作为转录后激活因子起作用,因为已证明通过不依赖CRM1的核输出信号进行核质穿梭是其对基因表达产生刺激作用的先决条件。基于这些发现,我们开展了研究以调查pUL69在mRNA输出中的作用,并证明pUL69能有效促进未剪接RNA的细胞质积累。此外,我们表明这种pUL69活性通过与高度相关的DEXD/H盒RNA解旋酶UAP56和URH49直接蛋白相互作用与细胞mRNA输出机制相关联。特别地,我们在pUL69的N末端鉴定出一个12个氨基酸的结构域,它是与UAP56和URH49结合所必需的,并且我们能够证明UAP56相互作用和核质穿梭都是pUL69介导的mRNA输出的先决条件。因此,我们鉴定出一个新的细胞靶点,它为疱疹病毒调节蛋白提供了进入保守细胞转运系统的途径,以促进未剪接RNA的核输出。

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