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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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TL;DR: The glnA gene of Rhodobacter sphaeroides encoding glutamine synthetase (GS) has been cloned and sequenced and molecular analysis revealed that there is a glnB gene upstream ofglnA, in a single glnBA operon.
Abstract: The glnA gene of Rhodobacter sphaeroides encoding glutamine synthetase (GS) has been cloned and sequenced. Molecular analysis revealed that there is a glnB gene upstream of glnA, in a single glnBA operon. A putative glnAp1-type promoter sequence, a consensus ntrC gene product binding site and a consensus upstream activator sequence were detected upstream of the glnB gene. The deduced amino acid sequences of the GS and GlnB proteins of R. sphaeroides showed strong homology with the same proteins from other Gram-negative bacteria. The sequence of the glnA gene isolated from glutamine auxotroph Gln83 was also determined. The glnA83 mutation was shown to result in premature termination of GS synthesis and formation of a 17 kDa C-truncated GS which could be complemented by a 5′-truncated glnA gene which encodes a 30 kDa N-truncated GS. This phenomenon is characteristic for interallelic complementation.

25 citations

Journal ArticleDOI
TL;DR: The positively acting MAL1R protein was also found to play a role in catabolite repression of MAL6T and Mal6S, and has an asymmetric effect on MAL gene expression, having a greater affect on MALT than on MALS.
Abstract: Maltose utilization in yeast requires the presence of any one of the five unlinked, homologous MAL loci. Transcription of the two structural genes MALT (permease) and MALS (maltase) is induced by maltose and catabolite-repressed by glucose. MAL6T and MAL6S share a common 5′ intergenic sequence; deletion studies within this sequence revealed a bi-directionally functioning upstream activation sequence (UASM) consisting of four 11bp homologous sites. Activation of these sites by the MALR protein results in the coordinate expression of MAL6T and MAL6S. The basal promoter activates MALS expression to a greater extent than MALT and is located in a region that overlaps UASM. Deletion of several subsites within the UASM has an asymmetric effect on MAL gene expression, having a greater affect on MALT than on MALS. Catabolite repression of MAL6T and MAL6S by glucose is controlled at several levels. Using disruption mutants, the positively acting MAL1R protein was also found to play a role in catabolite repression of MAL6T and MAL6S.

25 citations

Journal ArticleDOI
TL;DR: The pilE gene of Neisseria gonorrhoeae is transcribed from a sigma70 promoter (pilEp1) with an AT-rich tract extending 65 nucleotides upstream of the -35 box, which is an integration host factor (IHF)-binding core consensus sequence.
Abstract: The pilE gene of Neisseria gonorrhoeae is transcribed from a sigma70 promoter (pilEp1) with an AT-rich tract extending 65 nucleotides upstream of the -35 box. Within this region is an integration host factor (IHF)-binding core consensus sequence. We have performed a detailed analysis to determine which upstream sequences are required for efficient transcription from pilEp1 in N. gonorrhoeae. Deletion of sequences upstream of the AT-rich tract had no effect on the level of transcription. However, the IHF-binding core consensus sequence and the AT-rich sequence further upstream were both required for enhanced levels of transcription from this promoter in both N. gonorrhoeae and an Escherichia coli strain producing IHF. In addition, an UP-like element positioned between the -35 box and the IHF-binding site was required for maximal transcription. The AT-rich region upstream of the IHF-binding core consensus sequence can also act as an UP-like element when appropriately repositioned upstream of the -35 box.

25 citations

Journal ArticleDOI
TL;DR: The promoter of the FBP1 gene from Saccharomyces cerevisiae is identified, which codes for fructose-1,6-bisphosphatase and two elements which can form specific DNAprotein complexes and which confer glucose-repressed expression to an heterologous reporter gene.

25 citations

Journal ArticleDOI
TL;DR: These studies have characterized regions of the CR2 promoter and the transcription factors that bind to them and are crucial to induced CR2 expression and may provide insights to novel approaches to modulate B cell function by regulating CR2 gene transcription.
Abstract: Complement receptor 2 (CR2) is regulated at the transcriptional level, but the promoter elements and the transcription factors that bind to them and contribute to its regulation are unknown. After documenting that PMA and cAMP induced the activity of the CR2 promoter by 10-fold, we conducted promoter truncation and mutagenesis experiments, in conjunction with shift assays, to determine the functionally important regions of the promoter and the proteins that bind to them. We identified two regions, separated by approximately 900 nucleotides, which together were responsible for inducible promoter activity. Mutagenesis of single promoter elements demonstrated a functional upstream stimulatory factor/E box in the TATA box-proximal region and three equally important, closely spaced, CREB/AP-1 half-sites in the upstream promoter region. The cAMP response element-binding protein (CREB)/AP-1 half-sites bound in vitro Jun and CREB that are induced by protein kinases A and/or C. The 900-nucleotide segment stretching between the above two regions had no functional impact on the induced transcription, and its deletion increased the promoter activity. Finally, a region upstream of the distal site had a repressor activity on CR2 transcription. Moreover, IL-4 induced binding of CREB and AP-1 to the upstream promoter elements and resulted in increased CR2 surface protein expression. These studies have characterized regions of the CR2 promoter and the transcription factors that bind to them and are crucial to induced CR2 expression. Our studies may provide insights to novel approaches to modulate B cell function by regulating CR2 gene transcription.

25 citations


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