Trans-activation by human immunodeficiency virus tat protein requires the C-terminal domain of RNA polymerase II

被引:88
作者
Okamoto, H
Sheline, CT
Corden, JL
Jones, KA
Peterlin, BM
机构
[1] UNIV CALIF SAN FRANCISCO,HOWARD HUGHES MED INST,DEPT MED,SAN FRANCISCO,CA 94143
[2] UNIV CALIF SAN FRANCISCO,HOWARD HUGHES MED INST,DEPT MICROBIOL,SAN FRANCISCO,CA 94143
[3] UNIV CALIF SAN FRANCISCO,HOWARD HUGHES MED INST,DEPT IMMUNOL,SAN FRANCISCO,CA 94143
[4] SALK INST BIOL STUDIES,LA JOLLA,CA 92037
[5] JOHNS HOPKINS UNIV,SCH MED,DEPT MOL BIOL & GENET,BALTIMORE,MD 21210
关键词
D O I
10.1073/pnas.93.21.11575
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Human immunodeficiency virus (HIV)encoded trans-activator (Tat) acts through the transactivation response element RNA stem-loop to increase greatly the processivity of RNA polymerase II. Without Tat, transcription originating from the HIV promoter is attenuated. In this study, we demonstrate that transcriptional activation by Tat in vivo and in vitro requires the C-terminal domain (CTD) of RNA polymerase II. In contrast, the CTD is not required for basal transcription and for the formation of short, attenuated transcripts. Thus, trans-activation by Tat resembles enhancer-dependent activation of transcription. These results suggest that effects of Tat on the processivity of RNA polymerase II require proteins that are associated with the CTD and may result in the phosphorylation of the CTD.
引用
收藏
页码:11575 / 11579
页数:5
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