Luo Y, Madore S J, Parslow T G, Cullen B R, Peterlin B M
Howard Hughes Medical Institute, University of California, San Francisco 94143.
J Virol. 1993 Sep;67(9):5617-22. doi: 10.1128/JVI.67.9.5617-5622.1993.
Transcriptional trans-activation of the human immunodeficiency virus type 1 long terminal repeat requires that the virally encoded Tat effector interacts with its target trans-activation response element (TAR) RNA stem-loop. Although the arginine-rich region of Tat from amino acids 49 to 59 is sufficient to bind to TAR RNA in vitro, the RNA-binding domain of Tat has not been defined in vivo. Human immunodeficiency virus type 1 also encodes the Rev protein, which acts through an RNA stem-loop called the Rev-response element to transport unspliced and singly spliced viral RNA species from the nucleus to the cytoplasm. To map the RNA-binding domain of Tat, we performed assays that relied on Rev function using the heterologous RNA-tethering mechanism of Tat and the TAR. By examining the effects of selected targeted mutations of Tat on the abilities of hybrid Tat/Rev proteins to rescue the expression of unspliced mRNA via the TAR, we demonstrated that residues throughout the N-terminal 59 amino acids of Tat are required for binding of Tat and TAR RNA in vivo.
人类免疫缺陷病毒1型长末端重复序列的转录反式激活要求病毒编码的Tat效应蛋白与其靶标反式激活应答元件(TAR)RNA茎环相互作用。尽管Tat中从氨基酸49至59的富含精氨酸区域在体外足以与TAR RNA结合,但Tat的RNA结合结构域在体内尚未明确。人类免疫缺陷病毒1型还编码Rev蛋白,该蛋白通过一种称为Rev应答元件的RNA茎环发挥作用,将未剪接和单剪接的病毒RNA种类从细胞核转运至细胞质。为了绘制Tat的RNA结合结构域,我们利用Tat和TAR的异源RNA拴系机制进行了依赖Rev功能的检测。通过检查Tat的选定靶向突变对杂交Tat/Rev蛋白通过TAR拯救未剪接mRNA表达能力的影响,我们证明Tat N端59个氨基酸中的所有残基在体内对于Tat与TAR RNA的结合都是必需的。