ArticleGenetics2001
Multiple functions of the nonconserved N-terminal domain of yeast TATA-binding protein.
Article in Genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 33 citations in OpenAlex.
- Functional divergence of TBP homologs through distinct DNA-binding dynamics.Nucleic acids research · 2025Article
- Stress tolerance enhancement via SPT15 base editing in Saccharomyces cerevisiae.Biotechnology for biofuels · 2021Article
- Influence of the N-terminal domain and divalent cations on self-association and DNA binding by the Saccharomyces cerevisiae TATA binding protein.Biochemistry · 2007Article
- Shutoff of RNA polymerase II transcription by poliovirus involves 3C protease-mediated cleavage of the TATA-binding protein at an alternative site: incomplete shutoff of transcription interferes with efficient viral replication.Journal of virology · 2005Article
- Mutational analysis of BTAF1-TBP interaction: BTAF1 can rescue DNA-binding defective TBP mutants.Nucleic acids research · 2005Article
- Structural and functional analysis of mutations along the crystallographic dimer interface of the yeast TATA binding protein.Molecular and cellular biology · 2003Article
- Mot1 associates with transcriptionally active promoters and inhibits association of NC2 in Saccharomyces cerevisiae.Molecular and cellular biology · 2002Article
- A TATA binding protein mutant with increased affinity for DNA directs transcription from a reversed TATA sequence in vivo.Molecular and cellular biology · 2002Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The TATA-binding protein (TBP) is composed of a highly conserved core domain sufficient for TATA-element binding and preinitiation complex formation as well as a highly divergent N-terminal region that is dispensable for yeast cell viability. In vitro, removal of the N-terminal region domain enhances TBP-TATA association and TBP dimerization. Here, we examine the effects of truncation of the N-terminal region in the context of yeast TBP mutants with specific defects in DNA binding and in interactions with various proteins. For a subset of mutations that disrupt DNA binding and the response to transcriptional activators, removal of the N-terminal domain rescues their transcriptional defects. By contrast, deletion of the N-terminal region is lethal in combination with mutations on a limited surface of TBP. Although this surface is important for interactions with TFIIA and Brf1, TBP interactions with these two factors do not appear to be responsible for this dependence on the N-terminal region. Our results suggest that the N-terminal region of TBP has at least two distinct functions in vivo. It inhibits the interaction of TBP with TATA elements, and it acts positively in combination with a specific region of the TBP core domain that presumably interacts with another protein(s).
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.