Lu X, Welsh T M, Peterlin B M
Howard Hughes Medical Institute, University of California, San Francisco 94143-0724.
J Virol. 1993 Apr;67(4):1752-60. doi: 10.1128/JVI.67.4.1752-1760.1993.
The human immunodeficiency virus type 1 long terminal repeat sets up two different transcription complexes, which have been called processive and nonprocessive complexes. By mutating and substituting cis-acting sequences, we mapped elements of the human immunodeficiency virus long terminal repeat that are responsible for creating each transcription complex. Whereas processive complexes are efficiently assembled by upstream promoter elements in the absence of the TATA box, nonprocessive complexes absolutely require the TATA box. Moreover, the TATA box alone can set up these nonprocessive complexes, and nonprocessive but not processive complexes are trans activated by Tat. Finally, a strong DNA-binding site between the TATA box and trans-activation-responsive region interferes with either the assembly or movement of these nonprocessive complexes and diminishes the effects of Tat. Thus, Tat affects a critical step in the formation of elongation-competent transcription complexes.
1型人类免疫缺陷病毒长末端重复序列建立了两种不同的转录复合物,分别称为进行性和非进行性复合物。通过对顺式作用序列进行突变和替换,我们绘制了人类免疫缺陷病毒长末端重复序列中负责创建每种转录复合物的元件。在没有TATA框的情况下,进行性复合物可由上游启动子元件有效组装,而非进行性复合物则绝对需要TATA框。此外,单独的TATA框即可建立这些非进行性复合物,并且非进行性而非进行性复合物可被Tat反式激活。最后,TATA框与反式激活应答区域之间的一个强DNA结合位点会干扰这些非进行性复合物的组装或移动,并减弱Tat的作用。因此,Tat影响了具有延伸能力的转录复合物形成过程中的一个关键步骤。