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Upstream activating sequence

About: Upstream activating sequence is a research topic. Over the lifetime, 1633 publications have been published within this topic receiving 100112 citations.


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Journal ArticleDOI
01 Jan 1985-Gene
TL;DR: The nucleotide sequence of the MEL1 gene of Saccharomyces carlsbergensis and the N-terminal amino acid sequence of its extracellular gene product, alpha-galactosidase (melibiase) (alpha-Gal) are determined.

59 citations

Journal ArticleDOI
TL;DR: Results indicate that upstream regulatory factors are not required for the in vivo binding of TFIID to the CYC1 promoter and that binding of tfiID to DNA is not necessarily a rate-limiting step in the activation of transcription in cells.
Abstract: Functional transcription initiation complexes can be assembled in vitro without the aid of regulatory factors that bind to upstream activating sequences. However, promoters that lack upstream activating sequences are transcribed poorly if at all in vivo, suggesting that regulatory factors are necessary for the assembly of transcription initiation complexes in cells. To test this possibility, we asked whether the general transcription factor TFIID can bind to a promoter in yeast that lacks upstream activating sequences and is transcriptionally inactive. Analysis of an inactive CYC1 core promoter by high-resolution genomic footprinting revealed efficient binding of TFIID to either of two TATA box elements. Addition of a heat shock element rendered this promoter highly responsive to induction of transcription by heat shock but did not alter the TATA box footprints in the core promoter. Inactivation of all but one TATA box by site-directed mutagenesis did not prevent TFIID from binding to the remaining wild-type TATA box independently of regulatory sequences. These results indicate that upstream regulatory factors are not required for the in vivo binding of TFIID to the CYC1 promoter and that binding of TFIID to DNA is not necessarily a rate-limiting step in the activation of transcription in cells. Differences in chromatin structure may account for why regulatory transcription factors are required for the binding of TFIID to some promoters but not to others.

59 citations

Journal ArticleDOI
TL;DR: It is argued that Gln3p is capable of direct UAS(NTR) binding and participates in transcriptional activation of NCR-sensitive genes.
Abstract: When readily used nitrogen sources are available, the expression of genes encoding proteins needed to transport and metabolize poorly used nitrogen sources is repressed to low levels; this physiological response has been designated nitrogen catabolite repression (NCR). The cis-acting upstream activation sequence (UAS) element UAS(NTR) mediates Gln3p-dependent, NCR-sensitive transcription and consists of two separated dodecanucleotides, each containing the core sequence GATAA. Gln3p, produced in Escherichia coli and hence free of all other yeast proteins, specifically binds to wild-type UAS(NTR) sequences and DNA fragments derived from a variety of NCR-sensitive promoters (GDH2, CAR11 DAL3, PUT1, UGA4, and GLN1). A LexA-Gln3 fusion protein supported transcriptional activation when bound to one or more LexAp binding sites upstream of a minimal CYC1-derived promoter devoid of UAS elements. LexAp-Gln3p activation of transcription was largely independent of the nitrogen source used for growth. These data argue that Gln3p is capable of direct UAS(NTR) binding and participates in transcriptional activation of NCR-sensitive genes.

59 citations

Journal ArticleDOI
TL;DR: In vitro footprint analysis revealed that spo0A protein bound to two locations in the spo0F promoter region, consistent with a hypothesis that Spo0A binding to this region is responsible for activating Spo0F transcription.
Abstract: The spo0F gene of Bacillus subtilis encodes a protein that functions as a secondary messenger in a phosphorelay system controlling the initiation of sporulation. Transcription of the spo0F gene was known to be dependent on an intact gene for the transcription regulator Spo0A. In vitro footprint analysis revealed that Spo0A protein bound to two locations in the spo0F promoter region. Deletion of a 40 bp region upstream of one of the promoters (P2) abolished the activation of spo0F expression that occurs at the onset of stationary phase and sporulation. This 40 bp region contains a Spo0A-binding site. These observations are consistent with a hypothesis that Spo0A binding to this region is responsible for activating spo0F transcription. Additionally, Spo0A binding at a downstream site could modulate the level of this activation. Since Spo0F protein is required for the formation of Spo0A-P (the form needed for transcriptional activation) a positive feedback loop controls transcription of spo0F.

59 citations

Journal ArticleDOI
TL;DR: The possibility that the regulation of expression of p53 occurs, in part, by means of a potential HLH-containing factor provides a possible mechanism for the suppression of proliferation by the MyoD family of transcriptional regulators.
Abstract: Expression of the p53 gene plays an important role in the regulation of cellular proliferation and malignant transformation. Overexpression of mutant forms of p53 is in fact a common feature of many transformed cells. Studies dealing with the transcriptional regulatory regions of the p53 gene indicate that, unlike most promoters transcribed by RNA polymerase II, the p53 promoter contains no TATA-like sequence upstream of the transcription start site. Here we demonstrate that the murine p53 promoter contains a cis-acting element that maps downstream to the transcription initiation site. The integrity of this element is required for high-level expression from the promoter in transformed cells. By DNase I protection and mobility-shift analysis, we show that a nuclear factor binds to this downstream element through the consensus recognition sequence for the helix-loop-helix (HLH)-containing proteins of the myc/MyoD family of transcriptional regulators. We propose that the activity of one or more members of this family of transcription factors is an important determinant in the expression of p53 and that at least one level of p53 overexpression in transformed cells may thus be due to aberrant expression of the relevant factor(s). Furthermore, the possibility that the regulation of expression of p53 occurs, in part, by means of a potential HLH-containing factor provides a possible mechanism for the suppression of proliferation by the MyoD family of transcriptional regulators.

59 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20232
20223
20218
20206
20196
20186