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FEBS Lett. 2014 May 2;588(9):1630-6. doi: 10.1016/j.febslet.2014.01.067. Epub 2014 Mar 6.

7SK small nuclear ribonucleoprotein complex is recruited to the HIV-1 promoter via short viral transcripts.

Author information

1
Division of Host-Parasite Interaction, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan; Laboratory of Basic Science, Institute of Microbial Chemistry;BIKAKEN, 3-14-23 Kamiosaki, Shinagawa-ku, Tokyo 141-0021, Japan; RNA and Biofunctions, Precursory Research for Embryonic Science and Technology (PRESTO), Japan Science and Technology Agency (JST), 4-1-8 Honcho, Kawaguchi, Saitama 332-0012, Japan. Electronic address: mizutanit@bikaken.or.jp.
2
Division of Host-Parasite Interaction, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan; Laboratory of Basic Science, Institute of Microbial Chemistry;BIKAKEN, 3-14-23 Kamiosaki, Shinagawa-ku, Tokyo 141-0021, Japan.
3
Department of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, 5-1-5 Kashiwanoha, Kashiwa-shi, Chiba 277-8568, Japan.
4
Division of Host-Parasite Interaction, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.

Abstract

In this study, we demonstrate that the 7SK small nuclear ribonucleoprotein (snRNP) complex is recruited to the HIV-1 promoter via newly-synthesized HIV-1 nascent transcripts (short transcripts) in an hnRNP A1-dependent manner and negatively regulates viral transcript elongation. Our deep-sequence analysis showed these short transcripts were mainly arrested at approximately +50 to +70 nucleotides from the transcriptional start site in the U1 cells, an HIV-1 latent model. TNF-α treatment promptly disrupted the 7SK snRNP complex on the nascent transcripts and viral elongated transcripts were increased. This report provides insight into how 7SK snRNP complex is recruited to HIV-1 promoter in the absence of Tat.

KEYWORDS:

Chromatin regulation; Molecular biology; RNA virus; Viral transcription; Virology

PMID:
24607481
DOI:
10.1016/j.febslet.2014.01.067
[Indexed for MEDLINE]
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