Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20226 (TATA-binding protein)
 1,297 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies demonstrated that mutations in the Saccharomyces cerevisiae NOT genes increase transcription from TATA-less promoters. In this report, I show that in contrast, mutations in the yeast MOT1 gene decrease transcription from TATA-less promoters. I also demonstrate specific genetic interactions between the Not complex, Mot1p, and another global regulator of transcription in S. cerevisiae, Spt3p. Five distinct genetic interactions have been established. First, a null allele of SPT3, or a mutation in SPT15 that disrupts the interaction between Spt3p and TATA-binding protein (TBP), allele specifically suppressed the not1-2 mutation. Second, in contrast to not mutations, mutations in MOT1 decreased HIS3 and HIS4 TATA-less transcription. Third, not mutations suppressed toxicity due to overexpression of TBP in mot1-1 mutants. Finally, overexpression of SPT3 caused a weak Not- mutant phenotype in mot1-1 mutants. Collectively, these results suggest a novel type of transcriptional regulation whereby the distribution of limiting TBP (TFIID) on weak and strong TBP-binding core promoters is regulated: Mot1p releases stably bound TBP to allow its redistribution to low-affinity sites, and the Not proteins negatively regulate the activity of factors such as Spt3p that favor distribution of TBP to these low-affinity sites.
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PMID:The NOT, SPT3, and MOT1 genes functionally interact to regulate transcription at core promoters. 894 21

The assembly of transcription complexes at eukaryotic promoters involves a number of distinct steps including chromatin remodeling, and recruitment of a TATA-binding protein (TBP)-containing complexes, the RNA polymerase II holoenzyme. Each of these stages is controlled by both positive and negative factors. In this review, mechanisms that regulate the interactions of TBP with promoter DNA are described. The first is autorepression, where TBP sequesters its DNA-binding surface through dimerization. Once TBP is bound to DNA, factors such as TAF(II)250 and Mot1 induce TBP to dissociate, while other factors such as NC2 and the NOT complex convert the TBP/DNA complex into an inactive state. TFIIA antagonizes these TBP repressors but may be effective only in conjunction with the recruitment of the RNA polymerase II holoenzyme by promoter-bound activators. Taken together, the ability to induce a gene may depend minimally upon the ability to remodel chromatin as well as alleviate direct repression of TBP and other components of the general transcription machinery. The magnitude by which an activated gene is expressed, and thus repeatedly transcribed, might depend in part on competition between TBP inhibitors and the holoenzyme for access to the TBP/TATA complex.
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PMID:Control of gene expression through regulation of the TATA-binding protein. 1097 59