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At least 91 records · Page 5Linked to original sources
PubMed1996

TATA box and Sp1 sites mediate the activation of c-myc promoter P1 by immunoglobulin kappa enhancers.

In Burkitt's lymphoma (BL) cells the proto-oncogene c-myc is transcriptionally activated by chromosomal translocation to the immunoglobulin (Ig) gene loci. This activation is characterized by preferential transcription from the c-myc promoter P1 and accomplished by juxtaposed Ig enhancer elements. To identify promoter elements required for enhancer-activated P1 transcription, we studied the activation of c-myc reporter gene constructs by the Ig kappa intron and 3' enhancers. Deletion analysis defined the core promoter with a TATA box and two adjacent GC/GT boxes upstream sufficient for basal and enhancer-activated transcription. Gel retardation assays revealed Sp1's binding affinity to the GC/GT box proximal to the TATA box to be higher than to the distal one. This difference correlated well with the resulting levels of transcription mediated by Sp1 in contransfection experiments in BL and Sp1-deficient SL2 cells. Sp3 also bound to the core promoter in vitro, but failed to transactivate in vivo. Mutation of the distal Sp1 site moderately affected basal transcription concomitant with a modest decrease in enhancer stimulation. Mutation of the proximal Sp1 site almost entirely abolished basal as well as enhanced transcription. A considerable level of basal transcription was maintained upon mutation of the TATA box, whereas enhancer-activated transcription largely was abolished. Stable transfection of the BL cell line Raji with constructs containing core promoter mutations confirmed that the proximal Sp1 site and the TATA box are essential for the activation of promoter P1 by the Ig kappa enhancers.

Burkitt Lymphoma↗
PubMed1988

A yeast activity can substitute for the HeLa cell TATA box factor.

Most class B (II) promoter regions from higher eukaryotes contain the TATA box and upstream and enhancer elements. Both the upstream and enhancer elements and their cognate factors have regulatory functions, whereas the TATA sequence interacts with the TATA box factor BTF1 to position RNA polymerase B and its ancillary initiation factors (STF, BTF2 and BTF3) to direct the initiation of transcription approximately 30 base pairs downstream. In many respects, class B promoter regions from the unicellular eukaryote Saccharomyces cerevisiae are similarly organized, containing upstream activating sequences that bear many similarities to enhancers. Although they are essential for initiation, the yeast TATA sequences are located at variable distances and further from the start sites (40-120 base pairs), whose locations are primarily determined by an initiator element. The basic molecular mechanisms that control initiation of transcription are known to be conserved from yeast to man: the yeast transcriptional transactivator GAL4 can activate a minimal TATA box-containing promoter in human HeLa cells, and a human inducible enhancer factor, the oestrogen receptor, can activate a similar minimal promoter in yeast. This striking evolutionary conservation prompted us to look for the presence in yeast of an activity that could possibly substitute for the human TATA box factor. We report here the existence of such an activity in yeast extracts.

Base Sequence↗
PubMed1998

Contributions of the TATA box sequence to rate-limiting steps in transcription initiation by RNA polymerase II.

We have examined the role of the TATA box in determining transcription initiation frequency in vitro by studying a collection of promoters containing different TATA sequences in the context of the adenovirus major late promoter. In addition to measuring transcription rates, we have determined how the sequence changes affected the association and dissociation kinetics and the affinity of TBP binding. We observed that transcription from promoters containing the highest affinity TATA boxes is limited by the rate with which TBP associates with the promoter. In contrast, transcription from promoters containing lower affinity TATA boxes appears to be limited both by how much TBP is bound and by the relatively low occupancy of the conformation that can undergo subsequent steps in preinitiation complex assembly. The implications of these results in understanding the mechanism of transcription enhancement by transcriptional activators is discussed.

Adenoviridae↗
PubMed2005

Phenylephrine requires the TATA box to activate transcription of GLUT1 in neonatal rat cardiac myocytes.

Cardiac hypertrophy and heart failure occur in association to alterations in glucose uptake and metabolism. Phenylephrine, among other hypertrophic agonists, has been reported to increase expression of GLUT1 in neonatal rat cardiac myocytes by activating transcription. However, the specific cis- or trans-acting factors in the GLUT1 gene that are targeted by this agonist remain elusive. Here we describe that the activity of the -99/+134 basal promoter of rat GLUT1 is increased by phenylephrine. Nevertheless, this is not mediated by previously described binding sites (GC-box, MG1E) in the promoter. Rather, the TATA box is required by the agonist to activate transcription from the promoter. Interestingly, The Ras-ERK mitogen-activated protein (MAP) kinase pathway is involved in the actions of phenylephrine on GLUT1 transcription, and the effects of Ras on the activity of the promoter depend on the integrity of the TATA box. Our data indicate that phenylephrine induces the expression of the TBP-associated factor TAF(II)250 mRNA, which increases in parallel to the expression of GLUT1, suggesting that altering the expression of basal transcription factors could be one mechanism by which phenylephrine may regulate the activity of the GLUT1 promoter.

Animals↗
PubMed1993

Targeting TBP to a non-TATA box cis-regulatory element: a TBP-containing complex activates transcription from snRNA promoters through the PSE.

In the human small nuclear RNA (snRNA) promoters, the presence of a TATA box recognized by the TATA box-binding protein (TBP) determines the selection of RNA polymerase III over RNA polymerase II. The RNA polymerase II snRNA promoters are, therefore, good candidates for TBP-independent promoters. We show here, however, that TBP activates transcription from RNA polymerase II snRNA promoters through a non-TATA box element, the snRNA proximal sequence element (PSE), as part of a new snRNA-activating protein complex (SNAPc). In contrast to the previously identified TBP-containing complexes SL1, TFIID, and TFIIIB, which appear dedicated to transcription by a single RNA polymerase, SNAPc is also essential for RNA polymerase III transcription from the U6 snRNA promoter. The U6 initiation complex appears to contain two forms of TBP, one bound to the TATA box and one bound to the PSE as a part of SNAPc, suggesting that multiple TBP molecules can have different functions within a single promoter.

Animals↗
PubMed2001

The roles of two TATA boxes and 3'-flanking region of soybean beta-tubulin gene (tubB1) in light-sensitive expression.

The soybean tubB1 gene is expressed primarily in the germinating seedling and is strongly down regulated in response to light in the upper hypocotyl. Previous studies demonstrate that the 1 kb 5'-flanking region of this gene is sufficient for its appropriate expression in etiolated seedlings. Transient expression studies demonstrated that the presence of the tubB1 3'-flanking sequence element decreased reporter gene expression as compared to the nopaline synthase (NOS) 3'-flanking sequence element. In this study we investigated the ability of the 3' flanking region to influence the expression of a beta-glucuronidase (GUS) reporter gene in transgenic tobacco and Arabidopsis. The presence of the tubB1 3'-flanking sequence element in chimera constructs reduced reporter gene expression specifically in the hypocotyl and petioles of light-grown, transgenic seedlings. Additionally, site-directed mutagenesis of the two TATA sequences in the 1 kb tubB1 5'-flanking sequence element (TATA box A in the -122 to -117 bp region and TATA box B in the -35 to -30 region) showed that both elements are functional and additive in controlling tubB1 gene expression in seedling tissues. While transcription from TATA box A was predominant regardless of lighting conditions, the relative usage of TATA box B increased in the dark. We conclude that both TATA box sequences are utilized to direct expression of the tubB1 gene to the cotyledons, hypocotyl and root tip of germinating seedlings that are regions of cell expansion and that the 3'-flanking sequence element down-regulates expression in the hypocotyl in response to light. Thus, it is plausible that the tubB1 protein may play an important role in cell expansion in seedling development requiring its regulated expression by light.

Arabidopsis↗
PubMed1997

Cross-competition for TATA-binding protein between TATA boxes of the selenocysteine tRNA[Ser]Sec promoter and RNA polymerase II promoters.

In this study we show that the TATA-binding protein (TBP) interacts with the selenocysteine tRNA[Ser]Sec TATA element in a fashion analogous to the TBP-TATA interaction in RNA polymerase (Pol) II-transcribed genes even though the gene is transcribed by Pol III. Recombinant TBPs expressed in Escherichia coli bound to the tRNA[Ser]Sec TATA element. A factor was detected in Xenopus oocyte extracts which contain TBP and bind to the TATA boxes of the tRNA[Ser]Sec gene and various class II genes. Transcription of the microinjected tRNA[Ser]Sec gene was inhibited in Xenopus oocytes by coinjection with the TATA box of the adenovirus major late promoter (AdMLP). Transcription of a 5S gene was not affected under these conditions. These results suggest that the tRNA[Ser]Sec gene recruits TBP in a manner similar to that of TATA-dependent Pol II-transcribed genes and differently from that of Pol III-transcribed genes lacking a TATA box.

Animals↗
PubMed1994

Effects of minor groove binding drugs on the interaction of TATA box binding protein and TFIIA with DNA.

TBP (TATA box binding protein), a general transcription factor required for proper initiation of gene expression by RNA polymerase II, and minor groove binding drugs (MGBs) both interact with DNA within the minor groove at AT sites. This study has evaluated MGBs as inhibitors of DNA/TBP complex formation by gel mobility shift assays. Our results demonstrate that reversible MGBs (DAPI, distamycin A, Hoechst 33258, and netropsin) are effective inhibitors of the formation of DNA/TBP complex and that distamycin A is the most potent (0.16 microM inhibits TBP complex formation by 50%). CC-1065, a drug that covalently binds to DNA in the minor groove, is even more active than distamycin A (0.00085 microM inhibits TBP complex formation by 50%). Significantly more CC-1065 (0.009 microM) is required to break up preformed DNA/TBP complex compared to the drug concentration needed to prevent complex formation. In comparison, the order of drug addition has little influence on the ability of reversible MGBs to disrupt DNA/TBP complex. In the presence of TFIIA, a factor that enhances TBP association with DNA, greater drug concentrations (distamycin A and CC-1065, respectively) are needed to disrupt a preformed complex of DNA/TBP/TFIIA. In comparison to MGBs, drugs capable of binding to DNA by intercalation are generally weaker at blocking TBP complex formation except for hedamycin, which can intercalate and irreversibly bind to DNA and is as effective as reversible MGBs.

Base Sequence↗
PubMed1995

Activation functions of transcription factor Sp1 at U2 snRNA and TATA box promoters.

To localize regions in the human transcription factor Sp1, which are involved in activating transcription of the U2 snRNA gene promoter and of a TATA box gene promoter, the activation potentials of GAL4/Sp1 chimeras were analyzed in mammalian cells. In vitro mutagenesis analysis of Sp1 showed that mutation of a hydrophobic amino acid residue in glutamine-rich activation domain A impairs stimulation of transcription from the TATA box promoter, but not from the U2 promoter. Furthermore, we found that similar parts of Sp1 are involved in synergistic activation of transcription together with the SV40 enhancer and with an enhancer which binds a single type of transcription factor. This suggests that the activating mechanism of Sp1 is the same with both enhancers. Interestingly, we found that the glutamine-rich domains A and B, that stimulate transcription from the TATA box promoter were not sufficient for U2 gene activation. Stimulation of U2 transcription required amino acid residues 231-485 of Sp1, which contain the glutamine-rich domain B and a serine/threonine-rich part. Since overlapping, but non-identical parts of Sp1 are required for activation of the two promoter types, we conclude that Sp1 activates the U2 snRNA and TATA box promoters by different mechanisms.

Base Sequence↗
PubMed1992

Parvovirus H-1 P38 promoter requires the trans-activation region (tar), an SP1 site, and a TATA box for full activity.

In the parvovirus H-1 P38 promoter, there are sequences identified as a TATA box, an SP1 site, and a trans-activation responsive element (tar). It was previously shown that the parvovirus H-1 nonstructural protein NS1 positively regulates the expression of the P38 promoter for the viral capsid protein gene via the tar. To characterize the tar element further, a series of single-point mutations of the tar was constructed and the mutants were compared to wild-type for the trans-activation of the P38 promoter using a cat reporter gene. Most of the tar mutations had a negative effect on the P38 promoter and some of them reduced activity as much as 70%. However, when several mutants with multiple-point mutations in the tar were tested, no significant additive effect was observed. We examined the function of the SP1 site in the trans-activation of the P38 promoter by replacing the wild-type SP1 sequence with synthetic DNA fragments, OSP1 or 2SP1, containing no SP1 or two SP1 sites respectively, in a P38 construct with a cat reporter gene. The results indicate that P38 expression varies in proportion to the number of SP1 sites, suggesting a role for the SP1 site during trans-activation by NS1. The role of the TATA box on the P38 promoter was also examined by mutagenizing TATA to CACG. The activity of this promoter was reduced to 43%. When a construct mutated at both the SP1 and TATA box sites was tested for its activity, about 22% of the wild-type activity remained, implying that this remaining activity was contributed largely by the tar element. A model is proposed for how the tar element activates the wild-type and SP1-TATA minus promoters in the presence of NS1.

Base Sequence↗
PubMed1985

Functional analysis of a beta-globin gene containing a TATA box mutation from a Kurdish Jew with beta thalassemia.

We recently reported a TATA box mutation (ATAAAA to ATACAA) in a cloned beta-globin gene from a Kurdish Jew with homozygous beta thalassemia (Poncz, M., Ballantine, M., Solowiejczyk, D., Barak, I., Schwartz, E., and Surrey, S. (1982) J. Biol. Chem. 257, 5994-5996). We have now introduced this gene into HeLa cells after CaPO4 precipitation of the DNA and studied expression by analyzing globin-gene transcripts with a novel S1 nuclease mapping assay. Quantitative and qualitative comparison with the normal beta-globin gene revealed a promoter-down phenotype in the TATA box mutant, with normal RNA processing, and a normal start site for initiation of the primary transcript. Decreased transcriptional efficiency was confirmed directly by analysis of run-off transcripts using assays in vitro. The patient's phenotype of beta thalassemia major is probably the result of two different mutations since haplotype analysis of the beta-like globin gene clusters in genomic DNA from this patient shows heterozygosity for the Mediterranean-type haplotypes I and VII, with the TATA box mutation on a haplotype I chromosomal background.

Base Sequence↗
PubMed1988

A specific 15-bp TATA box promoter element is required for expression of a herpes simplex virus type 1 late gene.

The herpes simplex virus type 1 (HSV-1) glycoprotein C (gC) gene is a true late or gamma 2 gene in that its expression shows a strict requirement for viral DNA replication. Elements required for regulated expression of this gene were previously shown to consist of the gC TATA box, transcription start site and a large portion of the leader sequence of the gC gene. In this paper we show that transcription of the gC gene requires a 15-bp sequence, GGGTATAAATTCCGG, which contains the gC TATA box. This sequence contains specific promoter elements because replacement of this sequence with either the TATA box of the HSV-1 early thymidine kinase (tk) gene or two random TATA-like elements results in a transcriptionally inactive gC gene. In addition, we show that temporal expression of HSV beta and gamma genes at early and late times during infection are controlled by separate and distinct regulatory elements; regulatory signals distal to the TATA box are needed for early expression, whereas a gC-like TATA box is needed for late expression. These signals were identified by construction of a chimeric HSV gene that contained the distal control signals of the beta tk gene fused upstream of the TATA sequence of the gamma 2 gC gene. When RNA was isolated at various times postinfection from cells infected with a virus whose genome contained this chimeric tk-gC gene, synthesis of gC mRNA showed both early and late kinetics.

Base Sequence↗
PubMed1995

Role of the TATA box in transcription of the mouse mammary tumor virus long terminal repeat.

An in vitro transcription system from mammary cells was established to study transcription of the long terminal repeat (LTR) of the mouse mammary tumor virus (MMTV). Experiments with progressive 5'-deletion constructs of the MMTV LTR revealed that a 19-base pair (bp) region from -41 to -23 bp, encompassing the TATA box and flanking DNA sequence, was as transcriptionally active as larger promoter constructs, both in nuclear extracts from human mammary cell lines (T47D and MCF7) and a nonmammary cell line (HeLa). The cell-free system was capable of supporting transcriptional induction by factors binding upstream of the TATA box, however, since purified glucocorticoid receptor-induced transcription in larger promoter constructs encompassing the MMTV hormone-responsive elements. Transcription from two other promoters, the adenovirus major late promoter and the human immunodeficiency virus LTR, also revealed a significant transcriptional contribution of upstream elements. The 19-bp TATA region from the MMTV LTR was shown to have considerably more activity in this transcription system than comparable TATA regions from other promoters. Sequences critical to the MMTV TATA region were evaluated by single base pair mutagenesis and found to comprise a consensus TATA box sequence, TATAAAA, as well as a single A just upstream of the TATAAAA sequence. Thus, the high level of basal transcription observed with the TATA region from MMTV is due to a perfect consensus TATA box sequence and a single base immediately 5' adjacent. It is likely that the high basal rate of transcription observed with this TATA box region on histone-free templates represents an inappropriate level of basal expression and that a complete evaluation of transactivation mechanisms in this system will require the recapitulation in vitro of the chromatin-mediated repressive state that exists in vivo.

Base Sequence↗
PubMed1991

Control regions of an archaeal gene. A TATA box and an initiator element promote cell-free transcription of the tRNA(Val) gene of Methanococcus vannielii.

To identify the DNA sequences required for initiation of transcription in archaea, the 5'-flanking region of the tRNA(Val) gene of Methanococcus vannielii was modified by deletions, restructuring and site-directed mutagenesis, and the tRNA encoding sequence was replaced by a fortuitous Escherichia coli sequence. The effects of these mutations on promoter function were tested in an homologous cell-free transcription system. The DNA region from position -35 to +9 relative to the transcription start site was sufficient for maximal initiation of cell-free transcription. Removal of the DNA region between -35 and -30 reduced initiation by a factor of 2. Deletions extending to position -24 almost completely abolished specific transcription. Analysis of 16 site-specific mutations in the region from -33 to +2 provided evidence that a conserved A + T-rich sequence (TATA box), centered at -25, is essential for initiation of transcription. Single point mutations in six positions of the TATA box reduced initiation of transcription from 0.2 to 0.01 of wild-type levels. A second conserved motif at the transcription start site (consensus ATGC) could be replaced by some sequences containing a pyrimidine-purine dinucleotide but appeared necessary for a maximal rate of gene transcription. Mutations altering the spacing between the two conserved elements demonstrated that initiation occurs at a strictly defined distance of 22 to 27 base-pairs downstream from the TATA box. Our results support the conclusion that the TATA box is the major DNA region mediating promoter recognition, influencing the efficiency of transcription and specifying the site of transcription initiation. This Methanococcus promoter element closely resembles in structure and function the TATA box of promoters of eukaryotic protein-encoding genes transcribed by RNA polymerase II.

Base Sequence↗
PubMed2002

Photosynthesis nuclear genes generally lack TATA-boxes: a tobacco photosystem I gene responds to light through an initiator.

The promoter architecture of the nuclear-encoded photosystem I genes was studied using a tobacco gene, psaDb, as a model case. Linker scanning mutations revealed that the psaDb promoter does not have a TATA box. Instead, pyrimidine-rich Initiator (Inr) elements that overlap the transcription start sites are essential for light-responsive transcription of this gene. When the psaDb promoter was mutated to have a TATA-box but no Inr, light-responsive transcription was impaired, indicating that the regulatory system of this gene prefers Inr to a TATA box. As very little is known about plant TATA-less promoters, we subsequently examined whether this promoter architecture is unique to psaDb. Computer analysis of 232 plant promoters revealed surprising features; the majority of photosynthesis nuclear genes lacked TATA boxes, although the frequency of the TATA-less promoters in non-photosynthesis genes was less than 10%. These results strongly suggest that TATA-independent transcription mechanisms play important roles in the regulated expression of photosynthesis nuclear genes.

5' Flanking Region↗
PubMed1996

Formation of a combined H-DNA/open TATA box structure in the promoter sequence of the human Na,K-ATPase alpha2 gene.

Structural variation of DNA within the promoter of the human Na, K-ATPase alpha2 gene, which contains a 35-base pair (bp) homopyrimidine.homopurine (Py.Pu) tract adjacent to a TATA box has been studied. The Py.Pu tract contains a 26-bp quasi-mirror repeat sequence with a potential for intramolecular triplex formation. As analyzed by two-dimensional agarose gel electrophoresis, a plasmid containing 151 bp of the promoter sequence including the 35-bp Py.Pu tract undergoes structural transitions under moderately acidic pH. Chemical probing with chloroacetaldehyde, dimethyl sulfate, and potassium permanganate is consistent with the formation of triplex DNA within the Py.Pu tract at native superhelical density as isolated from Escherichia coli. Chemical probing was used to determine a supercoil dependence for the formation of this combined unwound structure. At the superhelical density sufficient to locally unwind DNA, an H-y3 isomer of intermolecular triplex likely forms. However, at higher superhelical tension an H-y5 structure forms in the Py.Pu tract, and with increasing supercoiling the local DNA unwinding extends into the abutting TATA box. The H-y5/open TATA box combination structure might be favorable at higher superhelical densities since it relaxes more supercoils. The possible involvement of the H-y5/open TATA box structure in transcription is discussed.

Base Sequence↗
PubMed2000

A role of transcriptional activators as antirepressors for the autoinhibitory activity of TATA box binding of transcription factor IID.

The TATA box-binding activity of transcription factor IID (TFIID) is autoinhibited by the N-terminal domain of the Drosophila TATA box-binding protein- (TBP) associated factor 230/yeast TBP-associated factor 145 subunit, which binds to the TATA box-binding domain of TBP by mimicking the TATA box structure. Here, we propose a mechanism of transcriptional activation that involves antirepression of this autoinhibitory activity by transcriptional activators. Like the autoinhibitory domain of TFIID, various acidic activators interact with the TATA box-binding domain of TBP. Moreover, the autoinhibitory domain of TFIID, which is known to interact with only the TATA box-binding domain of TBP, acts as an activation domain when fused to the GAL4 DNA-binding domain, indicating that interaction with the TATA-binding domain of TBP is crucial for activation of transcription. In a reciprocal fashion, the acidic activation domains can function as the autoinhibitory domain when the latter is replaced by the former within TFIID. These results indicate that activation domains and the autoinhibitory domain of TFIID are interchangeable, supporting a role for transcriptional activators as antirepressors of the autoinhibitory activity of the TATA box binding of TFIID.

Amino Acid Sequence↗
PubMed1994

Cooperativity in vivo between the E2 transactivator and the TATA box binding protein depends on core promoter structure.

The E2 transactivator protein of bovine papillomavirus 1 (BPV-1) can strongly stimulate complex promoters such as that of the herpes simplex virus thymidine kinase gene but does not efficiently activate minimal promoters that only contain E2 binding sites and a TATA box. Here we show that overexpression of the human, but not yeast, TATA box binding protein (TBP) in transfection experiments overcomes this block and enables E2 to activate a minimal TATA box-containing promoter. This suggests that recruitment of the TFIID complex to such promoters is normally a rate limiting step for transcriptional activation by E2 in vivo. In contrast, minimal promoters that contain an initiator element in addition to a TATA box are efficiently activated by E2 on its own and this activation is only moderately enhanced by TBP overexpression. In such E2-responsive promoters the TATA box or initiator can be functionally replaced by SP1 binding sites. Both the initiator binding protein, TFII-I, and SP1 have been found to interact physically with components of the TFIID complex. Since either TBP overexpression or the presence of an initiator or SP1 binding sites can increase activation by E2, it seems likely that the principal role of the E2 activation domain is to affect a step in the formation of the transcription initiation complex that occurs after TFIID has bound to the promoter. Sequential action of transcription factors, such as TFII-I, SP1 and E2, may be one type of mechanism underlying the widely observed phenomenon of transcriptional synergy.

Adenoviridae↗