A yeast TATA-binding protein mutant that selectively enhances gene expression from weak RNA polymerase II promoters

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Published inMolecular and Cellular Biology Vol. 17; no. 5; pp. 2888 - 2896
Main Authors Blair, Wade S., Cullen, Bryan R.
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.05.1997
Taylor & Francis
Subjects
Binding Sites
DNA, Fungal - metabolism
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Gene Expression Regulation
Mutagenesis
Promoter Regions, Genetic
RNA Polymerase II - genetics
RNA, Messenger - metabolism
Saccharomyces cerevisiae
TATA Box
TATA-Box Binding Protein
Trans-Activators - metabolism
Transcription Factor TFIID
Transcription Factors - genetics
Transcription Factors - metabolism
Transcription Factors, TFII - genetics
Transcription Factors, TFII - metabolism
Transcription, Genetic
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Abstract Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to MCB .asm.org, visit: MCB       
AbstractList We describe a unique gain-of-function mutant of the TATA-binding protein (TBP) subunit of Saccharomyces cerevisiae TFIID that, at least in part, renders transcriptional transactivators dispensable for efficient mRNA expression. The yTBPN69S mutant enhances transcription from weaker yeast promoter elements by up to 50-fold yet does not significantly increase gene expression directed by highly active promoters. Therefore, this TBP mutant and transcriptional transactivators appear to affect a common rate-limiting step in transcription initiation. Consistent with the hypothesis that this step is TFIID recruitment, tethering of TBP to a target promoter via a heterologous DNA binding domain, which is known to bypass the need for transcriptional transactivators, also nullifies the enhancing effect exerted by the N69S mutation. These data provide genetic support for the hypothesis that TFIID recruitment represents a rate-limiting step in the initiation of mRNA transcription that is specifically enhanced by transcriptional transactivators.
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Author W S Blair
B R Cullen
AuthorAffiliation Department of Genetics, Duke University Medical Center, Durham, North Carolina 27710, USA
AuthorAffiliation_xml – name: Department of Genetics, Duke University Medical Center, Durham, North Carolina 27710, USA
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  surname: Blair
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  surname: Cullen
  fullname: Cullen, Bryan R.
  email: culle002@mc.duke.edu
  organization: Howard Hughes Medical Institute and Department of Genetics, Duke University Medical Center
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We describe a unique gain-of-function mutant of the TATA-binding protein (TBP) subunit of Saccharomyces cerevisiae TFIID that, at least in part, renders...
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SubjectTerms Binding Sites
DNA, Fungal - metabolism
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Gene Expression Regulation
Mutagenesis
Promoter Regions, Genetic
RNA Polymerase II - genetics
RNA, Messenger - metabolism
Saccharomyces cerevisiae
TATA Box
TATA-Box Binding Protein
Trans-Activators - metabolism
Transcription Factor TFIID
Transcription Factors - genetics
Transcription Factors - metabolism
Transcription Factors, TFII - genetics
Transcription Factors, TFII - metabolism
Transcription, Genetic
Title A yeast TATA-binding protein mutant that selectively enhances gene expression from weak RNA polymerase II promoters
URI http://mcb.asm.org/content/17/5/2888.abstract
https://www.tandfonline.com/doi/abs/10.1128/MCB.17.5.2888
https://www.ncbi.nlm.nih.gov/pubmed/9111361
https://search.proquest.com/docview/15969705
https://pubmed.ncbi.nlm.nih.gov/PMC232141
Volume 17
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