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The 7SK small nuclear RNA inhibits the CDK9/cyclin T1 kinase to control transcription

The 7SK small nuclear RNA inhibits the CDK9/cyclin T1 kinase to control transcription The human positive transcription elongation factor P-TEFb, consisting of a CDK9/cyclin T1 heterodimer, functions as both a general and an HIV-1 Tat-specific transcription factor 1,2 . P-TEFb activates transcription by phosphorylating RNA polymerase (Pol) II, leading to the formation of processive elongation complexes. As a Tat cofactor, P-TEFb stimulates HIV-1 transcription by interacting with Tat and the transactivating responsive (TAR) RNA structure located at the 5′ end of the nascent viral transcript 3 . Here we identified 7SK, an abundant and evolutionarily conserved small nuclear RNA (snRNA) of unknown function 4,5 , as a specific P-TEFb-associated factor. 7SK inhibits general and HIV-1 Tat-specific transcriptional activities of P-TEFb in vivo and in vitro by inhibiting the kinase activity of CDK9 and preventing recruitment of P-TEFb to the HIV-1 promoter. 7SK is efficiently dissociated from P-TEFb by treatment of cells with ultraviolet irradiation and actinomycin D. As these two agents have been shown to significantly enhance HIV-1 transcription and phosphorylation of Pol II (refs 6,7,8), our data provide a mechanistic explanation for their stimulatory effects. The 7SK/P-TEFb interaction may serve as a principal control point for the induction of cellular and HIV-1 viral gene expression during stress-related responses. Our studies demonstrate the involvement of an snRNA in controlling the activity of a Cdk–cyclin kinase. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Springer Journals

The 7SK small nuclear RNA inhibits the CDK9/cyclin T1 kinase to control transcription

Yang, Zhiyuan; Zhu, Qingwei; Luo, Kunxin; Zhou, Qiang
Nature , Volume 414 (6861) – Nov 15, 2001
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References (24)

Publisher
Springer Journals
Copyright
Copyright © 2001 by Macmillan Magazines Ltd.
Subject
Science, Humanities and Social Sciences, multidisciplinary; Science, Humanities and Social Sciences, multidisciplinary; Science, multidisciplinary
ISSN
0028-0836
eISSN
1476-4687
DOI
10.1038/35104575
Publisher site
See Article on Publisher Site

Abstract

The human positive transcription elongation factor P-TEFb, consisting of a CDK9/cyclin T1 heterodimer, functions as both a general and an HIV-1 Tat-specific transcription factor 1,2 . P-TEFb activates transcription by phosphorylating RNA polymerase (Pol) II, leading to the formation of processive elongation complexes. As a Tat cofactor, P-TEFb stimulates HIV-1 transcription by interacting with Tat and the transactivating responsive (TAR) RNA structure located at the 5′ end of the nascent viral transcript 3 . Here we identified 7SK, an abundant and evolutionarily conserved small nuclear RNA (snRNA) of unknown function 4,5 , as a specific P-TEFb-associated factor. 7SK inhibits general and HIV-1 Tat-specific transcriptional activities of P-TEFb in vivo and in vitro by inhibiting the kinase activity of CDK9 and preventing recruitment of P-TEFb to the HIV-1 promoter. 7SK is efficiently dissociated from P-TEFb by treatment of cells with ultraviolet irradiation and actinomycin D. As these two agents have been shown to significantly enhance HIV-1 transcription and phosphorylation of Pol II (refs 6,7,8), our data provide a mechanistic explanation for their stimulatory effects. The 7SK/P-TEFb interaction may serve as a principal control point for the induction of cellular and HIV-1 viral gene expression during stress-related responses. Our studies demonstrate the involvement of an snRNA in controlling the activity of a Cdk–cyclin kinase.

Journal

Nature – Springer Journals

Published: Nov 15, 2001

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