Diversity of acetylation targets and roles in transcriptional regulation: the human immunodeficiency virus type 1 promoter as a model system

被引:40
作者
Quivy, V [1 ]
Van Lint, C [1 ]
机构
[1] Free Univ Brussels, Mol Virol Lab, Serv Chim Biol, IBMM, B-6041 Gosselies, Belgium
关键词
HIV-1; transcription; chromatin; acetylation; trichostatin A; NF-kappa B;
D O I
10.1016/S0006-2952(02)01152-8
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Persuasive evidence has accumulated that reversible acetylation of proteins is key post-translational modification regulating transcription in eukaryotes. Deacetylase inhibitors (such as trichostatin A) modulate the expression of similar to2% of all cellular genes. We and others have demonstrated a marked transcriptional activation of the human immunodeficiency virus type 1 (HIV-1) promoter in response to deacetylase inhibitors. Deacetylation events seem to be an important mechanism of HIV-1 transcriptional repression during latency, whereas acetylation events play critical functional roles in HIV-1 reactivation from latency. These deacetylation/acetylation events are implicated in chromatin remodeling of the viral promoter region, as well as in modulating the functional properties of cellular and viral transcription factors binding to this promoter region. Thereby, the HIV-1 promoter constitutes a unique regulatory model system to study the complex relationship between acetylation processes and transcriptional activity. (C) 2002 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:925 / 934
页数:10
相关论文
共 134 条
[11]   TAT TRANS-ACTIVATES THE HUMAN IMMUNODEFICIENCY VIRUS THROUGH A NASCENT RNA TARGET [J].
BERKHOUT, B ;
SILVERMAN, RH ;
JEANG, KT .
CELL, 1989, 59 (02) :273-282
[12]   β-catenin-histone deacetylase interactions regulate the transition of LEF1 from a transcriptional repressor to an activator [J].
Billin, AN ;
Thirlwell, H ;
Ayer, DE .
MOLECULAR AND CELLULAR BIOLOGY, 2000, 20 (18) :6882-6890
[13]   Cooperation of Spl and p300 in the induction of the CDK inhibitor p21WAF1/CIP1 during NGF-mediated neuronal differentiation [J].
Billon, N ;
Carlisi, D ;
Datto, MB ;
van Grunsven, LA ;
Watt, A ;
Wang, XF ;
Rudkin, BB .
ONCOGENE, 1999, 18 (18) :2872-2882
[14]   SODIUM-BUTYRATE ACTIVATES HUMAN-IMMUNODEFICIENCY-VIRUS LONG TERMINAL REPEAT - DIRECTED EXPRESSION [J].
BOHAN, C ;
YORK, D ;
SRINIVASAN, A .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1987, 148 (03) :899-905
[15]   MUTATIONAL ANALYSIS OF SODIUM-BUTYRATE INDUCIBLE ELEMENTS IN THE HUMAN IMMUNODEFICIENCY VIRUS TYPE-I LONG TERMINAL REPEAT [J].
BOHAN, CA ;
ROBINSON, RA ;
LUCIW, PA ;
SRINIVASAN, A .
VIROLOGY, 1989, 172 (02) :573-583
[16]   HATs on and beyond chromatin [J].
Chen, HW ;
Tini, M ;
Evans, RM .
CURRENT OPINION IN CELL BIOLOGY, 2001, 13 (02) :218-224
[17]   Duration of nuclear NF-κB action regulated by reversible acetylation [J].
Chen, LF ;
Fischle, W ;
Verdin, E ;
Greene, WC .
SCIENCE, 2001, 293 (5535) :1653-1657
[18]   The histone acetyltransferase, hGCN5, interacts with and acetylates the HIV transactivator, Tat [J].
Col, E ;
Caron, C ;
Seigneurin-Berny, D ;
Gracia, J ;
Favier, A ;
Khochbin, S .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (30) :28179-28184
[19]   The human factors YY1 and LSF repress the human immunodeficiency virus type 1 long terminal repeat via recruitment of histone deacetylase 1 [J].
Coull, JJ ;
Romerio, F ;
Sun, JM ;
Volker, JL ;
Galvin, KM ;
Davie, JR ;
Shi, Y ;
Hansen, U ;
Margolis, DM .
JOURNAL OF VIROLOGY, 2000, 74 (15) :6790-6799
[20]   Control of the histone-acetyltransferase activity of Tip60 by the HIV-1 transactivator protein, Tat [J].
Creaven, M ;
Hans, F ;
Mutskov, V ;
Col, E ;
Caron, C ;
Dimitrov, S ;
Khochbin, S .
BIOCHEMISTRY, 1999, 38 (27) :8826-8830