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PubMed1987

DNA sequences in the first intron of the human pro-alpha 1(I) collagen gene enhance transcription.

A chimeric gene was constructed in which sequences between 253 base pairs (bp) upstream of the start of transcription of the human pro-alpha 1(I) collagen gene and 117 bp downstream of that site were fused to the human alpha 1-globin gene, at a site immediately upstream of the globin initiation codon. Expression of this and subsequent chimeric gene constructions was investigated in microinjected Xenopus laevis oocytes. Presence of 253 bp of pro-alpha 1(I) collagen gene promoter sequences, containing a CAAT box and a TATA box, resulted in a relatively modest level of expression of the linked globin sequences. Lengthening of the pro-alpha 1(I) collagen gene promoter region to include 2400 bp of upstream sequences, increased transcription of the marker gene to some extent. Strong activation of transcription was obtained when a 782-bp fragment of the first intron of the collagen gene was introduced in chimeric constructions containing only 240 bp of the collagen promoter. An enhancing effect of the intron segment on expression of the marker gene was observed from downstream or upstream positions relative to the initiation site of transcription. Sequencing of the intron segment revealed the presence of four decanucleotide consensus sites for binding of the constitutive transcription factor Sp1, as well as an enhancer "core" motif. Our experiments also showed that the cis-acting region strongly enhance the activity of the pro-alpha 1(I) promoter in transfected fibroblasts. On the basis of these observations we conclude that the segment broadly located between +700 and +1300 in the first intron of the human pro-alpha 1(I) collagen gene contains cis-acting sequences with an enhancer effect on transcription of the gene.

Base Sequence↗
PubMed1988

Single copy gene for the chicken non-histone chromosomal protein HMG-17.

A chicken genomic library was screened with the human cDNA encoding the non-histone chromosomal protein HMG-17 and a 4565-base pair fragment containing the entire gene encoding this protein was isolated and characterized. Sequence analysis of the fragment revealed that from the start to end of transcription, the HMG-17 gene is 3293 base pairs long and is comprised of 6 exons ranging in size from 30 to 890 base pairs. Upstream of the putative cap site are both a CAAT box and a TATA box as well as several Sp1 binding sites. The gene has an extremely high content of G and C residues (75%) in a 1150-base pair fragment starting 500 base pairs from the putative cap site. This region satisfies the definition of an HpaII tiny fragment island. Southern analysis indicated that there is a single copy of this gene in chickens, whereas Northern analysis revealed that a single transcript is being synthesized from this gene. A comparison of the chicken and human cDNA and protein sequences and subsequent calculation of the evolutionary rates indicated that HMG-17 is a slowly evolving gene. The present article, which is the first study on the isolation and characterization of a complete gene coding for a high mobility group non-histone protein, indicates that the gene has features characteristic of housekeeping genes.

Amino Acid Sequence↗
PubMed1988

High-resolution analysis of the human gamma-globin gene promoter in K562 erythroleukemia cell chromatin.

We performed high-resolution mapping studies of the DNAse I-hypersensitive sites located just 5' to the human G gamma- and A gamma-globin genes of K562 erythroleukemia cells, in which these genes are constitutively expressed at low levels. This analysis revealed that the hypersensitive site extends from approximately -210 +/- 5 to -25 +/- 5 base pairs (bp) upstream from the transcription initiation site. Within this region, a GC-rich region located between the proximal CCAAT box and the TATA box is particularly accessible to nuclease digestion; however, the 5' end of the hypersensitive site is less accessible to nucleases. The pattern of DNAse I cleavage does not change on either strand with hemin induction of K562 cells, which increases the rate of gamma-globin gene transcription about threefold. The region within the hypersensitive site includes all the consensus promoter elements of the gamma-globin genes as well as an octamer sequence located between -182 and -175, and a region associated with a variety of mutations that may cause hereditary persistence of fetal hemoglobin (HPFH).

Chromatin↗
PubMed1998

Nucleotide structure and characterization of the murine gene encoding anticoagulant protein C.

The 15,160 bp murine gene encoding anticoagulation protein C (PC) was cloned and sequenced, including 414 bp upstream of exon 1 and 80 bp downstream of the translation stop codon. Nine exons and eight introns were identified. The first exon was untranslated and contained the major transcriptional start site, the surrounding nucleotide sequence of which matched reasonably well with the consensus eukaryotic Cap element sequence. The translational initiator methionine residue was located in exon 2. The other introns were positioned as splices between the major domain units of the protein. The 5' untranslated region contained two possible CCAAT sequences and GC boxes, but no TATA box was obvious within the optimal range of distances from the transcription start site. The 3'-flanking nucleotides included a probable polyadenylation site (ATTAAA), beginning 80 nucleotides downstream of the translation stop codon, and a downstream consensus sequence (AGTGTTTC) required for the efficient formation of a 3' terminus of mRNA. Several high probability transcription factor recognition sequences, including proteins that are enriched in, or specific to, the liver, such as C/EBP alpha, C/EBP beta, HNF1, and HNF3 beta, have been located in the 5' region of the gene. These results indicate that all elements are present for liver-based transcription of the gene for murine PC.

Amino Acid Sequence↗
PubMed1996

Heat shock factor gains access to the yeast HSC82 promoter independently of other sequence-specific factors and antagonizes nucleosomal repression of basal and induced transcription.

Transcription in eukaryotic cells occurs in the context of chromatin. Binding of sequence-specific regulatory factors must contend with the presence of nucleosomes for establishment of a committed preinitiation complex. Here we demonstrate that the high-affinity binding site for heat shock transcription factor (HSF) is occupied independently of other cis-regulatory elements and is critically required for preventing nucleosomal assembly over the yeast HSC82 core promoter under both noninducing (basal) and inducing conditions. Chromosomal mutation of this sequence, termed HSE1, erases the HSF footprint and abolishes both transcription and in vivo occupancy of the TATA box. Moreover, it dramatically reduces promoter chromatin accessibility to DNase I and TaqI, as the nuclease-hypersensitive region is replaced by a localized nucleosome. By comparison, in situ mutagenesis of two other promoter elements engaged in stable protein-DNA interactions in vivo, the GRF2/REB1 site and the TATA box, despite reducing transcription three- to fivefold, does not compromise the nucleosome-free state of the promoter. The GRF2-binding factor appears to facilitate the binding of proteins to both HSE1 and TATA, as these sequences, while still occupied, are less protected from in vivo dimethyl sulfate methylation in a deltaGRF2 strain. Finally, deletion of a consensus upstream repressor sequence (URS1), positioned immediately upstream of the GRF2-HSE1 region and only weakly occupied in chromatin, has no expression phenotype, even under meiotic conditions. However, deletion of URS1, like mutation of GRF2, shifts the translational setting of an upstream nucleosomal array flanking the promoter region. Taken together, our results argue that HSF, independent of and dominant among sequence-specific factors binding to the HSC82 upstream region, antagonizes nucleosomal repression and creates an accessible chromatin structure conducive to preinitiation complex assembly and transcriptional activation.

Base Sequence↗
PubMed1992

The functional importance of a cap site-proximal region of the human prointerleukin 1 beta gene is defined by viral protein trans-activation.

Prointerleukin 1 beta (IL-1 beta) is a cytokine that mediates a broad range of biological activities. Genomic sequences that regulate IL-1 beta transcription include both inducible regulatory elements located more than 2,700 bp upstream of the transcriptional start site (cap site) and proximal elements located near the TATA box of this gene. In this study, we focused on the identification and characterization of trans-acting nuclear regulatory proteins that bind to the cap site-proximal region of the human IL-1 beta gene. We identified a protein, termed NFIL-1 beta A (NF beta A), that binds to a highly conserved 12-bp DNA sequence (-49 to -38) located upstream of the TATA box motif in both the human and murine IL-1 beta genes. The IL-1 alpha gene, which lacks a TATA motif, does not possess an NF beta A-binding sequence within the promoter region, suggesting that NF beta A may selectively regulate IL-1 beta expression. Using electrophoretic mobility shift assays, we identified several distinct DNA-protein complexes that are expressed in a cell-type-specific manner. In monocytic cell lines, the relative abundance of these complexes varies rapidly following stimulation of the cells with phorbol esters or lipopolysaccharide. UV cross-linking analysis identified two distinct DNA-binding polypeptides that comprise distinct complexes. The functional role of NF beta A was assessed in transient transfection assays. These data indicate that NF beta A is required for both basal and inducible promoter activity in monocytic cells. Furthermore, the human cytomegalovirus immediate-early 1 gene product requires the presence of NF beta A in order to trans-activate the proximal IL-1 beta promoter in a monocytic cell line. We propose that NF beta A is a factor that mediates either direct or indirect activation by the immediate-early 1 gene product. The proximity of this essential factor to the TATA motif suggests a possible role in transcriptional initiation.

Animals↗
PubMed1997

Tandemly repeated 147 bp elements cause structural and functional variation in divergent MAL promoters of Saccharomyces cerevisiae.

We have studied four novel MAL promoters isolated from a single strain of bakers' yeast. Within these promoters we have identified up to five tandem 147 bp repeats located between the MAL UAS region and the MALT TATA box. These repeats strongly reduce MALT (maltose permease) gene expression but only weakly reduce MALS (maltase) gene expression. Insertion of the 147 bp elements into the heterologous CYC1 promoter reduced expression when located between the CYC1 UAS and the TATA box, but not when located upstream of the UAS. We propose that these naturally occurring repeats have evolved as a mechanism to lower the level of MALT expression relative of MALS expression, thus avoiding possible toxic effects associated with over-expression from multiple copies of the permease gene.

Base Sequence↗
PubMed1991

Lack of a requirement for strict rotational alignment among transcription factor binding sites in yeast.

The MF alpha 1 gene of Saccharomyces cerevisiae is an alpha specific gene whose expression is regulated by two upstream activation sites (UASMF alpha 1S), which are the binding sites for activator proteins, MAT alpha 1 and MCM1. UASMF alpha 1 elements act in a synergistic fashion; lack of either element causes reduced expression levels that are 6- to 45-fold less than that of intact promoter in alpha cells. We investigated the effect of manipulating rotational alignments among transcription factor binding sites of MF alpha 1 on the expression of the gene. The expression level of MF alpha 1 decreased with the spacing between the two UASMF alpha 1S and no synergism was observed when the distance of the two elements was longer than 90 base pairs. No strict rotational alignment was required for their synergistic action. We also show that the spacing between UASMF alpha 1 elements and TFIID binding site, the TATA box, had little, if any, effect on MF alpha 1 expression. We chose a sufficient number of positions for UASMF alpha 1S to ensure that, in several of these positions, MAT alpha 1 and MCM1 were on the opposite side of the DNA helix with respect to the TATA box.

Base Sequence↗
PubMed1997

Negative regulation of a heterologous promoter by human cytomegalovirus immediate-early protein IE2.

The HCMV IE2 protein promiscuously activates transcription of many viral and cellular genes. IE2 also negatively autoregulates its own expression by binding to a strategically positioned IE2 binding site, called CRS, located immediately downstream of the TATA box of the HCMV major IE promoter. Here we show that IE2 is able to repress transcription driven by a heterologous promoter, RSV LTR. Repression of RSV LTR by IE2 is completely dependent of DNA sequences downstream of the TATA box of RSV LTR. A DNA sequence, 5'-CGATACAATAAACG-3', evidently matching the proposed CRS consensus sequence, is located between nucleotides -13 and +1 (relative to the transcription start site) of RSV LTR. Three lines of evidence support the notion that this RSV CRS element is involved in the IE2-mediated repression of RSV LTR. First, introduction of mutation to the RSV CRS element renders to the mutant RSV LTR resistance to IE2-mediated repression. Second, a mutant IE2 defective in DNA binding cannot downregulate transcription from RSV LTR. Third, IE2 specifically binds to the wild-type, but not the mutant, RSV CRS element in vitro. These data, in conjunction with previous works, demonstrate that IE2 can passively repress transcription of homologous and heterologous promoters that contain a CRS element.

Cell Line↗
PubMed1995

TFIIIC determines RNA polymerase III specificity at the TATA-containing yeast U6 promoter.

The gene encoding yeast U6 snRNA that is transcribed by RNA polymerase III (Pol III) contains both a TATA box upstream of the transcription start site and a downstream binding site for the factor TFIIIC. This juxtaposition of elements typical of both Pol II- and Pol III-transcribed genes raises the question of how polymerase specificity is determined. The upstream U6 promoter containing the TATA box and transcription start site was shown previously to be transcribed by Pol III in vitro. We therefore tested whether the upstream promoter of yeast U6 encodes Pol III specificity. One model is that polymerase specificity is conferred by the homologous Pol II and Pol III transcription factors TFIIB and BRF1. However, we found no specificity in the binding of BRF1 or TFIIB to TATA-containing promoters of genes specifically transcribed by Pol III or Pol II. Yeast strains deficient for Pol II or Pol III transcription were employed to examine U6 polymerase specificity in vivo. We find that the U6 upstream promoter is Pol II-specific in vivo and is converted to Pol III specificity by TFIIIC. Thus, preferential recruitment of TFIIIB by TFIIIC probably excludes the Pol II general factors and promotes Pol III transcription, thereby determining polymerase specificity.

Base Sequence↗
PubMed1997

The promoter context is a decisive factor in establishing selective responsiveness to nuclear class II receptors.

The vigorous retinoic acid (RA)-dependent activation of the retinoic acid receptor beta2 (RARbeta2) gene in embryonal carcinoma (EC) cells is mediated by retinoid receptor heterodimers (RXR-RAR) binding to RAREs that are closely positioned to the TATA box and an EC cell-specific co-factor activity termed E1A-LA. Using a series of direct repeat (DR) elements, we now show that positioning RXR-RAR in close proximity to the basal transcription machinery assembled on the TATA box is decisive in RA responsiveness in EC cells. Notably, a DR1 element functions predominantly as an RAR-responsive element when placed in the context of the RARbeta2 promoter. Moreover, DR3 and DR4 elements which mediate vitamin D3 and thyroid hormone responses, respectively, in other contexts, are converted to exclusive RAR response elements when placed in the RARbeta2 promoter and EC cell context. In differentiated cells, the adenovirus E1A(13S) protein is required to achieve high level RA activation through all of the different DR elements placed in the RARbeta2 context, suggesting that the molecular bridging function of E1A-LA [E1A(13S)] is essential to redefining response element specificity. Finally, we show that the arrangement of cis-acting elements as present in the RARbeta2 promoter is not crucial, but rather the close positioning of the RAREs to the TATA. We conclude that the identity of a given cis-acting element is defined not only by its affinity for the transactivator, but also by the context in which it is placed, as well as the cell type in which the transactivator is expressed.

Adenovirus E1A Proteins↗
PubMed1998

Transcription of the juvenile hormone esterase gene under the control of both an initiator and AT-rich motif.

The binding of transcription factors to the core promoter of the juvenile hormone esterase gene was functionally characterized using both a cell-free in vitro transcription functional assay and a cell transfection assay. A core JHE promoter (-61 to +28 bp relative to transcription start site) supported faithful transcription from the in vivo transcription start site. The nuclear extracts from the Sf9 insect cell line that provided transcription from that template also bound to that template as a probe in gel-mobility shift assays. Deletion or transversion of the initiator-binding motif (-1 to +4 bp) abolished detectable transcription either in vitro or in transfected cells. An AT-rich motif (ATATAT; -28 to -23 bp) serves another transcription factor-binding site. Mutation of the AT-rich motif to a canonical TATA-box preserved transcription, while either its deletion or complete transversion abolished or significantly reduced detectable transcriptional activity. These results indicate that, under these conditions, the functional operation of this core promoter approaches that of a composite promoter in which both the TATA- and initiator-binding protein complexes are necessary, even for basal transcription. On the other hand, these debilitating mutations to either the TATA box or initiator motif did not prevent the ability of the corresponding gel-shift competitive probes to compete with the wild-type promoter for binding by the transcription factors. Even a double transversion of both the AT-rich motif and the initiator-binding motif was able to competitively displace the protein complex that bound to the labelled wild-type probe. These data strongly indicate the presence of (an) additional core-promoter-associated transcription factor(s) (that is not the 'downstream element') that contact(s) the AT-binding complex and/or initiator-binding factor with sufficient avidity to remove them from binding to the competing wild-type promoter sequence.

Animals↗
PubMed1998

TFII-I enhances activation of the c-fos promoter through interactions with upstream elements.

The transcription factor TFII-I was initially isolated as a factor that can bind to initiator elements in core promoters. Recent evidence suggests that TFII-I may also have a role in signal transduction. We have found that overexpression of TFII-I can enhance the response of the wild-type c-fos promoter to a variety of stimuli. This effect depends on the c-fos c-sis-platelet-derived growth factor-inducible factor binding element (SIE) and serum response element (SRE). There is no effect of cotransfected TFII-I on the TATA box containing the c-fos basal promoter. Three TFII-I binding sites can be found in c-fos promoter. Two of these overlap the c-fos SIE and SRE, and another is located just upstream of the TATA box. Mutations that distinguish between serum response factor (SRF), STAT, and TFII-I binding to the c-fos SIE and SRE suggest that the binding of TFII-I to these elements is important for c-fos induction in conjunction with the SRF and STAT transcription factors. Moreover, TFII-I can form in vivo protein-protein complexes with the c-fos upstream activators SRF, STAT1, and STAT3. These results suggest that TFII-I may mediate the functional interdependence of the c-fos SIE and SRE elements. In addition, the ras pathway is required for TFII-I to exert its effects on the c-fos promoter, and growth factor stimulation enhances tyrosine phosphorylation of TFII-I. These results indicate that TFII-I is involved in signal transduction as well as transcriptional activation of the c-fos promoter.

3T3 Cells↗
PubMed1993

Role of the negative glucocorticoid regulatory element in glucocorticoid repression of the human osteocalcin promoter.

In osteoblast-like cells in culture, the human osteocalcin gene promoter basal activity is repressed by glucocorticoids, reflecting the repression of serum osteocalcin concentrations noted in syndromes of glucocorticoid excess. 1,25-Dihydroxyvitamin D3 [1,25-(OH)2D3], the active hormonal form of vitamin D, induces the osteocalcin promoter through a vitamin D response element (VDRE), and glucocorticoids also repress the vitamin D-induced promoter. This study addresses the role of a glucocorticoid receptor (GR) binding site overlapping the TATA box of the osteocalcin promoter, which had been proposed as a negative glucocorticoid response element (nGRE), invoking a steric interference mechanism of glucocorticoid repression. Confirmation of the role of the nGRE in regulating basal activity was obtained using promoter constructs containing a TATA box swap. However, a minor component of repression of 1,25-(OH)2D3 induced activity remained in the absence of the nGRE. In addition, glucocorticoid repression of the human osteocalcin promotor was shown to be cell line specific. This result is not compatible with a simple model of repression and suggests the existence of unidentified cell-specific factors that are involved in the repression event. Repression of the osteocalcin promoter was compatible with a composite model involving both the nGRE site and glucocorticoid regulation of factors that bind the vitamin D response element.

Base Sequence↗
PubMed2005

Biochemical characterization of the human placental transcription factor GCMa/1.

Glial cells missing (GCM) proteins are a novel family of zinc-containing transcription factors. Human GCMa/1 is primarily expressed in placental trophoblast cells and regulates SYNCYTIN gene expression, which mediates fusion of cytotrophoblasts to form the syncytiotrophoblast layer of the human placenta. To biochemically characterize the transcriptional activity of GCMa/1, we set up an in vitro transcription system for human GCMa/1 (hGCMa/1). Using G-free reporter constructs carrying multiple copies of wild-type or mutant GCMa-binding site (GBS) in front of a synthetic TATA box, we observed specific transcriptional activities of recombinant hGCMa/1 proteins prepared from a baculovirus--insect cell or Escherichia coli expression system. We further characterized GCMa/1-mediated transcriptional activation on the native syncytin promoter. Using G-free reporter constructs containing the native syncytin promoter, a TATA box downstream of the proximal GBS in the syncytin promoter was shown to be essential for the transcription activation directed by hGCMa/1. Therefore, our results demonstrate positive transcriptional activities of GCMa/1 in vitro and provide a better understanding of GCMa/1-mediated SYNCYTIN gene expression.

Binding Sites↗
PubMed2004

Synergy of human Pol II core promoter elements revealed by statistical sequence analysis.

MOTIVATION: The subject of our paper is bioinformatics analysis of the distinguishing features of human promoter DNA sequences, in particular of synergetic combinations of core promoter elements therein. We suppose that specific scenarios of transcription initiation are essentially related to various particular implementations of the interaction of basal transcription machinery with promoter DNA, depending on the presence and mutual positioning of core promoter elements. RESULTS: In addition to the combinations of core promoter elements previously experimentally confirmed [TATA box and Initiator (Inr), Downstream Promoter Element (DPE) and Inr, and TFIIB recognition element (BRE) and TATA box] we propose other alternate synergetic combinations: BRE and Inr, BRE and DPE, and TATA and DPE with respective models. The suggestion is based on a high statistical significance of the alternate combinations in promoters, comparable with the significance of the known combinations. We also present arguments that the BRE element is statistically more important than previously thought, and suggest possible mechanisms of action of the core elements in the promoters with multiple transcription start sites. CONTACT: ioschikhes-1@medctr.osu.edu SUPPLEMENTARY INFORMATION: Supplementary information is available at http://bmi.osu.edu/~ilya/synergy/Gershenzon_SuppMat-R.pdf.

DNA Polymerase II↗
PubMed1992

Transcription from varicella-zoster virus gene 67 (glycoprotein IV).

Three transcripts map to the varicella-zoster virus (VZV) open reading frame (ORF) 67, which encodes glycoprotein IV (gpIV). All of these transcripts are polyadenylated and are transcribed from left to right towards the genomic terminal short repeats. Previous Northern (RNA) blot analyses suggested that the most abundant of these transcripts (1.65 kb) might code for gpIV. We performed S1 nuclease protection and primer extension assays and determined that the 5' terminus of the 1.65-kb transcript maps 91 bp upstream from the gpIV initiation codon. An AT-rich region (ATAAA), -28 bp from the cap site, is a potential TATA box, and at -71 bp there is a consensus CCAAT box motif. The 3' end of the 1.65-kb transcript is 20 bp downstream of two overlapping polyadenylation signals, AATAAA and ATTAAA, and just downstream of the 3' terminus is a GU-rich sequence. These results are reminiscent of data from our analysis of the VZV gpV gene, confirming that VZV appears able to use unusual TATA box motifs. Many canonical TATA sequences are present upstream from these VZV transcriptional start sites but, apparently, are not used. We tested sequences upstream from the gpIV cap site for promoter activity in transient expression experiments by cloning a DNA fragment (+63 to -343 bp) into pCAT3M, which contains a chloramphenicol acetyltransferase reporter gene. This clone showed little constitutive promoter activity but was activated more than 200-fold by infection with VZV and 5-fold with herpes simplex virus. The two known VZV transactivating genes (those for ORF 4 and ORF 62) were tested for their abilities to activate expression from the gpIV promoter by using their cognate promoters. The ORF 4 gene was minimally active, whereas the ORF 62 gene gave twofold induction; both genes, acting together, gave fivefold induction. However, replacement of the IE62 promoter with the immediate-early cytomegalovirus promoter in the ORF 62 construct gave over 40-fold induction of chloramphenicol acetyltransferase activity under the gpIV promoter in the same assay.

Amino Acid Sequence↗
PubMed1991

Identification of novel factors which bind specifically to the core promoter of the immunoglobulin heavy chain gene.

Nuclear extracts from HeLa cells and the B-cell line, BJA-B, generated two protein-DNA complexes which bound specifically to sequences in the TATA box of the immunoglobulin heavy chain gene (IgH) promoter. Complex A also bound the core promoter of a retroviral long terminal repeat but did not bind to five other promoters including the adenovirus major late promoter. Of these seven promoters, complex B bound only to the IgH promoter. Footprinting analysis revealed that both complexes A and B bound sequences which include the TATA element, and complex A additionally contacted sequences downstream to +28. Mutation of the IgH TATA element from ATTAATATA to GCTA-TAAAA, the optimal TATA sequence as found in the major late promoter, resulted in a 10-fold decrease in binding to complex A and a 25-fold decrease in binding complex B. Surprisingly, both transfection experiments in HeLa cells and in vitro transcription experiments with whole nuclear extract demonstrated that mutation of the TATA box in the core IgH promoter to this consensus sequence resulted in a 2-fold decrease in the level of transcription. These data suggest that the specific sequence of the TATA region is important, and factors which recognize these sequences, such as complex A and B, may modulate the level of transcription from the IgH promoter.

Base Sequence↗