A severely defective TATA-binding protein-TFIIB interaction does not preclude transcriptional activation in vivo

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A severely defective TATA-binding protein-TFIIB interaction does not preclude transcriptional activation in vivo.

In yeast cells, mutations in the TATA-binding protein (TBP) that disrupt the interaction with the TATA element or with TFIIA can selectively impair the response to acidic activator proteins. We analyzed the transcriptional properties of TBP derivatives in which residues that directly interact with TFIIB were replaced by alanines. Surprisingly, a derivative with a 50-fold defect in TBP-TFIIB-TAT...

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A new class of activation-defective TATA-binding protein mutants: evidence for two steps of transcriptional activation in vivo.

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Interdependent interactions between TFIIB, TATA binding protein, and DNA.

Temperature-sensitive mutants of TFIIB that are defective for essential interactions were isolated. One mutation (G204D) results in disruption of a protein-protein contact between TFIIB and TATA binding protein (TBP), while the other (K272I) disrupts an interaction between TFIIB and DNA. The TBP gene was mutagenized, and alleles that suppress the slow-growth phenotypes of the TFIIB mutants were...

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Increased recruitment of TATA-binding protein to the promoter by transcriptional activation domains in vivo.

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Transcriptional activation by TFIIB mutants that are severely impaired in interaction with promoter DNA and acidic activation domains.

Biochemical experiments indicate that the general transcription factor IIB (TFIIB) can interact directly with acidic activation domains and that activators can stimulate transcription by increasing recruitment of TFIIB to promoters. For promoters at which recruitment of TFIIB to promoters is limiting in vivo, one would predict that transcriptional activity should be particularly sensitive to TF...

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ژورنال

عنوان ژورنال: Molecular and Cellular Biology

سال: 1997

ISSN: 0270-7306,1098-5549

DOI: 10.1128/mcb.17.3.1336