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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The RNA element encoded by the trans-activation-responsive region of human immunodeficiency virus type 1 is functional when displaced downstream of the start of transcription.
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The RNA element encoded by the trans-activation-responsive region of human immunodeficiency virus type 1 is functional when displaced downstream of the start of transcription.

机译：由人类免疫缺陷病毒1型的反式激活应答区编码的RNA元件在转录开始的下游移位时起作用。

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摘要

The human immunodeficiency virus type 1 (HIV-1) trans-activator protein, Tat, specifically stimulates transcription from the viral long terminal repeat. Tat binds to an RNA stem-loop structure encoded by the trans-activation response region (TAR). To test whether TAR is functional when displaced downstream of the start of transcription, we assayed a series of templates carrying duplicated TAR elements in cell-free transcription systems. When the normally positioned TAR element (TAR-1) is inactivated by mutations in either the Tat binding site or the apical loop sequence, which acts as the binding site for a cellular factor, transactivation can be rescued by a wild-type TAR element placed downstream (TAR-2). The TAR-2 element is functional even when placed > 200 nt downstream of TAR-1. TAR complementation experiments have also shown that a functional TAR element requires both an intact Tat binding site and an intact apical loop sequence. For example, if TAR-1 carries a mutation in the loop element it cannot be rescued by a TAR-2 element carrying a mutation in the Tat binding site. Substitution mutations in TAR-1 show that the 5' half of TAR also encodes an essential DNA element which is required for efficient transcription initiation. These results strongly suggest that Tat and cellular cofactors which bind TAR RNA associate with the transcription complex during its transit through TAR.
机译：人类免疫缺陷病毒1型（HIV-1）反式激活蛋白Tat特异性刺激病毒长末端重复序列的转录。 Tat结合由反式激活反应区（TAR）编码的RNA茎环结构。为了测试TAR在转录开始下游时是否有功能，我们检测了一系列模板，这些模板在无细胞转录系统中带有重复的TAR元素。当正常定位的TAR元件（TAR-1）被Tat结合位点或顶端环序列（作为细胞因子的结合位点）突变而失活时，可以通过放置野生型TAR元件来挽救反式激活作用下游（TAR-2）。即使将TAR-2元件放置在TAR-1下游> 200 nt处，它也可以起作用。 TAR互补实验还表明，功能性TAR元件需要完整的Tat结合位点和完整的顶端环序列。例如，如果TAR-1在环元件中携带突变，则不能通过在Tat结合位点中携带突变的TAR-2元件来挽救。 TAR-1中的取代突变表明TAR的5'半部分还编码有效转录起始所需的必需DNA元件。这些结果强烈表明，结合TAR RNA的Tat和细胞辅助因子在转录复合物通过TAR的过程中与转录复合物结合。

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