GA-binding protein factors, in concert with the coactivator CREB binding protein/p300, control the induction of the interleukin 16 promoter in T lymphocytes

Bannert, Norbert; Avots, Andris; Baier, Michael; Serfling, Edgar; Kurth, Reinhard

doi:10.1073/pnas.96.4.1541

Cited by 56 publications

(43 citation statements)

References 46 publications

(39 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the presence of these regulatory proteins is apparently not sufficient to recruit either the HATs or GTFs to the IE promoters, since the recruitment was ineffective during RP5 infection. This conclusion is somewhat surprising, given evidence that CBP and p300 can interact in vitro with GABP and Sp1 (1,51,61). This reinforces the value of testing such interactions in an appropriate in vivo context.…”

Section: Discussionmentioning

confidence: 77%

VP16-Dependent Association of Chromatin-Modifying Coactivators and Underrepresentation of Histones at Immediate-Early Gene Promoters during Herpes Simplex Virus Infection

Herrera

Triezenberg

2004

J Virol

175

253

View full text Add to dashboard Cite

During infection by herpes simplex virus type 1 (HSV-1), the virion protein VP16 activates the transcription of viral immediate-early (IE) genes. Genetic and biochemical assays have shown that the potent transcriptional activation domain of VP16 can associate with general transcription factors and with chromatin-modifying coactivator proteins of several types. The latter interactions are particularly intriguing because previous reports indicate that HSV-1 DNA does not become nucleosomal during lytic infection. In the present work, chemical cross-linking and immunoprecipitation assays were used to probe the presence of activators, general transcription factors, and chromatin-modifying coactivators at IE gene promoters during infection of HeLa cells by wild-type HSV-1 and by RP5, a viral strain lacking the VP16 transcriptional activation domain. The presence of VP16 and Oct-1 at IE promoters did not depend on the activation domain. In contrast, association of RNA polymerase II, TATA-binding protein, histone acetyltransferases (p300 and CBP), and ATP-dependent remodeling proteins (BRG1 and hBRM) with IE gene promoters was observed in wild-type infections but was absent or reduced in cells infected by RP5. In contrast to the previous evidence for nonnucleosomal HSV-1 DNA, histone H3 was found associated with viral DNA at early times of infection. Interestingly, histone H3 was underrepresented on IE promoters in a manner dependent on the VP16 activation domain. Thus, the VP16 activation domain is responsible for recruiting general transcription factors and coactivators to IE promoters and also for dramatically reducing the association of histones with those promoters.The activation domain of VP16 (VP16 AD) from herpes simplex virus type I (HSV-1) has been widely used as a model for the study of transcriptional activation in eukaryotes. During infection, VP16 triggers the cascade of viral gene expression by activating transcription of the viral immediate-early (IE) genes (65). VP16 forms a DNA-binding complex with the cellular proteins Oct-1 and HCF-1 at specific cis elements present in the IE gene promoters (27,40,48,68). The potent VP16 AD (10, 55), often artificially fused to a heterologous DNA-binding domain (47), can activate transcription in a wide range of organisms, including yeasts, insects, plants, and mammals (3,47,58,66), indicating that mechanisms of transcriptional activation are broadly conserved through evolution.Interactions of the VP16 AD with general transcription factors (GTFs) including transcription factor IIB (TFIIB), TFIIH, TATA-binding protein (TBP), and TBP-associated factors (TAFs) suggest that the VP16 AD might activate transcription by stimulating the assembly of an RNA polymerase II (RNA Pol II) preinitiation complex (13,17,24,31,56,67). Consistent with this model, in vitro experiments have demonstrated the ability of the VP16 AD to promote the formation of the ternary complex formed by TFIIA, TFIID, and TATA box DNA (25). The VP16 AD might also recruit the RNA Pol II holoenzyme through i...

show abstract

Section: Discussionmentioning

confidence: 77%

VP16-Dependent Association of Chromatin-Modifying Coactivators and Underrepresentation of Histones at Immediate-Early Gene Promoters during Herpes Simplex Virus Infection

Herrera

Triezenberg

2004

J Virol

175

253

View full text Add to dashboard Cite

show abstract

“…Structural features of the DNA-protein contacts have been described for a direct repeat of core elements (6,28). On the other hand, a palindrome with the core elements directed in opposite directions, as in the IL-16 promoter, was shown to favor heterotetramer formation (4). A relative autonomy of the individual ␣␤ dimers on each site is suggested by the functional analysis of reporters carrying mutations in either fp1 or fp2 that showed additivity and not synergism of their activities (Fig.…”

Section: Discussionmentioning

confidence: 95%

Synergistic Action of GA-Binding Protein and Glucocorticoid Receptor in Transcription from the Mouse Mammary Tumor Virus Promoter

Aurrekoetxea-Hernández

Buetti

2000

J Virol

View full text Add to dashboard Cite

B lymphocytes are among the first cells to be infected by mouse mammary tumor virus (MMTV), and they play a crucial role in its life cycle. To study transcriptional regulation of MMTV in B cells, we have analyzed two areas of the long terminal repeat (LTR) next to the glucocorticoid receptor binding site, fp1 (at position ؊139 to ؊146 from the cap site) and fp2 (at ؊157 to ؊164). Both showed B-cell-specific protection in DNase I in vitro footprinting assays and contain binding sites for Ets transcription factors, a large family of proteins involved in cell proliferation and differentiation and oncogenic transformation. In gel retardation assays, fp1 and fp2 bound the heterodimeric Ets factor GA-binding protein (GABP) present in B-cell nuclear extracts, which was identified by various criteria: formation of dimers and tetramers, sensitivity to pro-oxidant conditions, inhibition of binding by specific antisera, and comigration of complexes with those formed by recombinant GABP. Mutations which prevented complex formation in vitro abolished glucocorticoid-stimulated transcription from an MMTV LTR linked to a reporter gene in transiently transfected B-cell lines, whereas they did not affect the basal level. Exogenously expressed GABP resulted in an increased level of hormone response of the LTR reporter plasmid and produced a synergistic effect with the coexpressed glucocorticoid receptor, indicating cooperation between the two. This is the first example of GABP cooperation with a steroid receptor, providing the opportunity for studying the integration of their intracellular signaling pathways.Mouse mammary tumor virus (MMTV) is a type B retrovirus which causes carcinomas of the mammary gland in females of susceptible mouse strains (8, 13). The carcinogenic transformation results from transcriptional activation of a particular class of cellular oncogenes (int genes; reviewed in reference 59). The mammary gland specificity of the oncogenic property of MMTV depends on the high viral replication rate and consequent high reinfection rate in the mammary epithelial cells, which are stimulated by pregnancy-related hormones. This hormonal stimulation has made the MMTV promoter the beststudied model for investigating the regulation of gene expression by steroid hormones (for a review, see references 7 and 51). Glucocorticoids, progesterone, and androgens (but not estrogens) strongly stimulate the rate of MMTV transcription through the binding of hormone-receptor complexes in the hormone regulatory element (HRE) (see Fig. 1) region of the proviral DNA, located upstream of the promoter in the long terminal repeat (LTR). Binding sites for additional transcription factors have been characterized, in particular for CTF (also called nuclear factor 1 [NF-1]) and Oct-1 in the HRE, and for mammary gland-specific factors further upstream in the LTR (reviewed in reference 31).During primary infection, MMTV is transmitted in the milk from the mother to the newborn and is taken up in the intestine, where it infects local lymphocytes (rev...

show abstract

“…The hormone affects gene expression by activating STATs (6,7). Additional transcription factors known to activate genes controlling androgen metabolism, inflammation, and energy homeostasis, such as GA-binding proteins (GABPs), also contribute to hepatic sexual dimorphism (8)(9)(10)(11)(12). Furthermore, epigenetic modifications, including DNA methylation and methylation-sensitive transcription factors, participate in male-specific gene expression.…”

Section: Introductionmentioning

confidence: 99%

Sumoylated PPARα mediates sex-specific gene repression and protects the liver from estrogen-induced toxicity in mice

Leuenberger¹,

Pradervand²,

Wahli³

2009

J. Clin. Invest.

102

View full text Add to dashboard Cite

As most metabolic studies are conducted in male animals, understanding the sex specificity of the underlying molecular pathways has been broadly neglected; for example, whether PPARs elicit sex-dependent responses has not been determined. Here we show that in mice, PPARα has broad female-dependent repressive actions on hepatic genes involved in steroid metabolism and immunity. In male mice, this effect was reproduced by the administration of a synthetic PPARα ligand. Using the steroid oxysterol 7α-hydroxylase cytochrome P450 7b1 (Cyp7b1) gene as a model, we elucidated the molecular mechanism of this sex-specific PPARα-dependent repression. Initial sumoylation of the ligand-binding domain of PPARα triggered the interaction of PPARα with GA-binding protein α (GABPα) bound to the target Cyp7b1 promoter. Histone deacetylase and DNA and histone methylases were then recruited, and the adjacent Sp1-binding site and histones were methylated. These events resulted in loss of Sp1-stimulated expression and thus downregulation of Cyp7b1. Physiologically, this repression conferred on female mice protection against estrogen-induced intrahepatic cholestasis, the most common hepatic disease during pregnancy, suggesting a therapeutic target for prevention of this disease.

show abstract

GA-binding protein factors, in concert with the coactivator CREB binding protein/p300, control the induction of the interleukin 16 promoter in T lymphocytes

Abstract: Interleukin 16

Cited by 56 publications

References 46 publications

VP16-Dependent Association of Chromatin-Modifying Coactivators and Underrepresentation of Histones at Immediate-Early Gene Promoters during Herpes Simplex Virus Infection

VP16-Dependent Association of Chromatin-Modifying Coactivators and Underrepresentation of Histones at Immediate-Early Gene Promoters during Herpes Simplex Virus Infection

Synergistic Action of GA-Binding Protein and Glucocorticoid Receptor in Transcription from the Mouse Mammary Tumor Virus Promoter

Sumoylated PPARα mediates sex-specific gene repression and protects the liver from estrogen-induced toxicity in mice

Contact Info

Product

Resources

About