ArticleMolecular and cellular biology1997
Role for ADA/GCN5 products in antagonizing chromatin-mediated transcriptional repression.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
85 citing papers in PubMed, 202 citations in OpenAlex.
- Species-Specific Transcription Factors Associated with Long Terminal Repeat Promoters of Endogenous Retroviruses: A Comprehensive Review.Biomolecules · 2024Review
- Ash1 and Tup1 dependent repression of the Saccharomyces cerevisiae HO promoter requires activator-dependent nucleosome eviction.PLoS genetics · 2020Article
- Characterization of a metazoan ADA acetyltransferase complex.Nucleic acids research · 2019Article
- Retrotransposon targeting to RNA polymerase III-transcribed genes.Mobile DNA · 2018Review
- Not5-dependent co-translational assembly of Ada2 and Spt20 is essential for functional integrity of SAGA.Nucleic acids research · 2017Article
- Article
- Structure and Functional Diversity of GCN5-Related N-Acetyltransferases (GNAT).International journal of molecular sciences · 2016Review
- Subunits of ADA-two-A-containing (ATAC) or Spt-Ada-Gcn5-acetyltrasferase (SAGA) Coactivator Complexes Enhance the Acetyltransferase Activity of GCN5.The Journal of biological chemistry · 2015Article
- The Ty1 LTR-retrotransposon of budding yeast,Microbiology spectrum · 2015Article
- Role of nucleosome remodeling in neurodevelopmental and intellectual disability disorders.Frontiers in behavioral neuroscience · 2015Review
- Chromatin dynamics: interplay between remodeling enzymes and histone modifications.Biochimica et biophysica acta · 2014Review
- Casein kinase 2 associates with the yeast chromatin reassembly factor Spt2/Sin1 to regulate its function in the repression of spurious transcription.Molecular and cellular biology · 2013Article
- Biochemical characterization of Hpa2 and Hpa3, two small closely related acetyltransferases from Saccharomyces cerevisiae.The Journal of biological chemistry · 2013Article
- Chromatin and transcription in yeast.Genetics · 2012Review
- Functional antagonism between Sas3 and Gcn5 acetyltransferases and ISWI chromatin remodelers.PLoS genetics · 2012Article
- Histone H3 tail acetylation modulates ATP-dependent remodeling through multiple mechanisms.Nucleic acids research · 2011Article
- Transcription regulation by the noncoding RNA SRG1 requires Spt2-dependent chromatin deposition in the wake of RNA polymerase II.Molecular and cellular biology · 2011Article
- Article
- Derepression of INO1 transcription requires cooperation between the Ino2p-Ino4p heterodimer and Cbf1p and recruitment of the ISW2 chromatin-remodeling complex.Eukaryotic cell · 2010Article
- Experimental approaches to the study of epigenomic dysregulation in ageing.Experimental gerontology · 2010Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The Saccharomyces cerevisiae SWI/SNF complex is a 2-MDa multimeric assembly that facilitates transcriptional enhancement by antagonizing chromatin-mediated transcriptional repression. We show here that mutations in ADA2, ADA3, and GCN5, which are believed to encode subunits of a nuclear histone acetyltransferase complex, cause phenotypes strikingly similar to that of swi/snf mutants. ADA2, ADA3, and GCN5 are required for full expression of all SWI/SNF-dependent genes tested, including HO, SUC2, INO1, and Ty elements. Furthermore, mutations in the SIN1 gene, which encodes a nonhistone chromatin component, or mutations in histone H3 or H4 partially alleviate the transcriptional defects caused by ada/gcn5 or swi/snf mutations. We also find that ada2 swi1, ada3 swi1, and gcn5 swi1 double mutants are inviable and that mutations in SIN1 allow viability of these double mutants. We have partially purified three chromatographically distinct GCN5-dependent acetyltransferase activities, and we show that these enzymes can acetylate both histones and Sin1p. We propose a model in which the ADA/GCN5 and SWI/SNF complexes facilitate activator function by acting in concert to disrupt or modify chromatin structure.
Indexed as
Identifiers
What OpenQuestion holds
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.