ArticleGenetics2010
Snf1p regulates Gcn5p transcriptional activity by antagonizing Spt3p.
Article in Genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Sucrose-nonfermenting 1 kinase activates histone acetylase GCN5 to promote cellulase production in Trichoderma.Applied microbiology and biotechnology · 2023Article
- Spt3 and Spt8 Are Involved in the Formation of a Silencing Boundary by Interacting with TATA-Binding Protein.Biomolecules · 2023Article
- Article
- Posttranslational regulation of the GCN5 and PCAF acetyltransferases.PLoS genetics · 2022Review
- Identification of Tension Sensing Motif of Histone H3 in Saccharomyces cerevisiae and Its Regulation by Histone Modifying Enzymes.Genetics · 2016Article
- Snf1-Dependent Transcription Confers Glucose-Induced Decay upon the mRNA Product.Molecular and cellular biology · 2016Article
- Muscle Wasting in Fasting Requires Activation of NF-κB and Inhibition of AKT/Mechanistic Target of Rapamycin (mTOR) by the Protein Acetylase, GCN5.The Journal of biological chemistry · 2015Article
- Sense and antisense transcription are associated with distinct chromatin architectures across genes.Nucleic acids research · 2015Article
- Glucose repression in Saccharomyces cerevisiae.FEMS yeast research · 2015Review
- Ptc1 protein phosphatase 2C contributes to glucose regulation of SNF1/AMP-activated protein kinase (AMPK) in Saccharomyces cerevisiae.The Journal of biological chemistry · 2013Article
- Nutritional control of growth and development in yeast.Genetics · 2012Review
- The AMP-activated protein kinase Snf1 regulates transcription factor binding, RNA polymerase II activity, and mRNA stability of glucose-repressed genes in Saccharomyces cerevisiae.The Journal of biological chemistry · 2012Article
- Integrated analysis of transcriptome and lipid profiling reveals the co-influences of inositol-choline and Snf1 in controlling lipid biosynthesis in yeast.Molecular genetics and genomics : MGG · 2012Article
- Snf1/AMPK regulates Gcn5 occupancy, H3 acetylation and chromatin remodelling at S. cerevisiae ADY2 promoter.Biochimica et biophysica acta · 2012Article
- Article
- The spliceosome-activating complex: molecular mechanisms underlying the function of a pleiotropic regulator.Frontiers in plant science · 2012Article
- Mapping the interaction of Snf1 with TORC1 in Saccharomyces cerevisiae.Molecular systems biology · 2011Article
- Glucose signaling-mediated coordination of cell growth and cell cycle in Saccharomyces cerevisiae.Sensors (Basel, Switzerland) · 2010Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The budding yeast Gcn5p is a prototypic histone acetyltransferase controlling transcription of diverse genes. Here we show that Gcn5p is itself regulated by Snf1p and Spt3p. Snf1p likely controls Gcn5p via direct interaction. Mutating four residues in the Gcn5p catalytic domain, T203, S204, T211, and Y212 (TSTY), phenocopies snf1 null cells, including Gcn5p hypophosphorylation, hypoacetylation at the HIS3 promoter, and transcriptional defects of the HIS3 gene. However, overexpressing Snf1p suppresses the above phenotypes associated with the phosphodeficient TSTY mutant, suggesting that it is the interaction with Snf1p important for Gcn5p to activate HIS3. A likely mechanism by which Snf1p potentiates Gcn5p function is to antagonize Spt3p, because the HIS3 expression defects caused by snf1 knockout, or by the TSTY gcn5 mutations, can be suppressed by deleting SPT3. In vitro, Spt3p binds Gcn5p, but the interaction is drastically enhanced by the TSTY mutations, indicating that a stabilized Spt3p-Gcn5p interaction may be an underlying cause for the aforementioned HIS3 transcriptional defects. These results suggest that Gcn5p is a target regulated by the competing actions of Snf1p and Spt3p.
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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.