ArticleGenetics2006
Genetic interactions between Nhp6 and Gcn5 with Mot1 and the Ccr4-Not complex that regulate binding of TATA-binding protein in Saccharomyces cerevisiae.
Article in Genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- ATAC-seq and MNase-seq Detect Distinct Modes of Chromatin Accessibility.bioRxiv : the preprint server for biology · 2026Article
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- The interplay between transcription and mRNA degradation inMicrobial cell (Graz, Austria) · 2017Review
- The Modifier of Transcription 1 (Mot1) ATPase and Spt16 Histone Chaperone Co-regulate Transcription through Preinitiation Complex Assembly and Nucleosome Organization.The Journal of biological chemistry · 2016Article
- Mot1 redistributes TBP from TATA-containing to TATA-less promoters.Molecular and cellular biology · 2013Article
- The control of elongation by the yeast Ccr4-not complex.Biochimica et biophysica acta · 2013Review
- RNA-binding protein Khd1 and Ccr4 deadenylase play overlapping roles in the cell wall integrity pathway in Saccharomyces cerevisiae.Eukaryotic cell · 2011Article
- FACT and Asf1 regulate nucleosome dynamics and coactivator binding at the HO promoter.Molecular cell · 2009Article
- A proteomics analysis of yeast Mot1p protein-protein associations: insights into mechanism.Molecular & cellular proteomics : MCP · 2008Article
- Article
- Article
- Requirement of Nhp6 proteins for transcription of a subset of tRNA genes and heterochromatin barrier function in Saccharomyces cerevisiae.Molecular and cellular biology · 2007Article
- The fate of the messenger is pre-determined: a new model for regulation of gene expression.Biochimica et biophysica actaReview
- Ccr4-Not complex: the control freak of eukaryotic cells.Critical reviews in biochemistry and molecular biologyReview
- Nhp6: a small but powerful effector of chromatin structure in Saccharomyces cerevisiae.Biochimica et biophysica actaReview
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous work suggests that the Nhp6 HMGB protein stimulates RNA polymerase II transcription via the TATA-binding protein TBP and that Nhp6 functions in the same functional pathway as the Gcn5 histone acetyltransferase. In this report we examine the genetic relationship between Nhp6 and Gcn5 with the Mot1 and Ccr4-Not complexes, both of which have been implicated in regulating DNA binding by TBP. We find that combining either a nhp6ab or a gcn5 mutation with mot1, ccr4, not4, or not5 mutations results in lethality. Combining spt15 point mutations (in TBP) with either mot1 or ccr4 also results in either a growth defect or lethality. Several of these synthetic lethalities can be suppressed by overexpression of TFIIA, TBP, or Nhp6, suggesting that these genes facilitate formation of the TBP-TFIIA-DNA complex. The growth defect of a not5 mutant can be suppressed by a mot1 mutant. HO gene expression is reduced by nhp6ab, gcn5, or mot1 mutations, and the additive decreases in HO mRNA levels in nhp6ab mot1 and gcn5 mot1 strains suggest different modes of action. Chromatin immunoprecipitation experiments show decreased binding of TBP to promoters in mot1 mutants and a further decrease when combined with either nhp6ab or gcn5 mutations.
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