ArticleMolecular and cellular biology2006
SWI/SNF binding to the HO promoter requires histone acetylation and stimulates TATA-binding protein recruitment.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 63 citations in OpenAlex.
- The nBAF complex subunit CREST/SS18L1 regulates hippocampal memory processes via tyrosine 397 and histone acetyltransferase CBP.Cell reports · 2026Article
- Ash1 and Tup1 dependent repression of the Saccharomyces cerevisiae HO promoter requires activator-dependent nucleosome eviction.PLoS genetics · 2020Article
- Capturing and Understanding the Dynamics and Heterogeneity of Gene Expression in the Living Cell.International journal of molecular sciences · 2020Review
- FACT and Ash1 promote long-range and bidirectional nucleosome eviction at the HO promoter.Nucleic acids research · 2020Article
- Article
- Multiple Negative Regulators Restrict Recruitment of the SWI/SNF Chromatin Remodeler to theGenetics · 2019Article
- Histone acetylation promotes long-lasting defense responses and longevity following early life heat stress.PLoS genetics · 2019Article
- Article
- The chromatin remodeler ZmCHB101 impacts expression of osmotic stress-responsive genes in maize.Plant molecular biology · 2018Article
- Article
- Understanding nucleosome dynamics and their links to gene expression and DNA replication.Nature reviews. Molecular cell biology · 2017Review
- Mechanisms of action and regulation of ATP-dependent chromatin-remodelling complexes.Nature reviews. Molecular cell biology · 2017Review
- Loss of Snf5 Induces Formation of an Aberrant SWI/SNF Complex.Cell reports · 2017Article
- Cooperation between SAGA and SWI/SNF complexes is required for efficient transcriptional responses regulated by the yeast MAPK Slt2.Nucleic acids research · 2016Article
- Nucleosomes Are Essential for Proper Regulation of a Multigated Promoter in Saccharomyces cerevisiae.Genetics · 2016Article
- Role of nucleosome remodeling in neurodevelopmental and intellectual disability disorders.Frontiers in behavioral neuroscience · 2015Review
- Dancing the cell cycle two-step: regulation of yeast G1-cell-cycle genes by chromatin structure.Trends in biochemical sciences · 2013Review
- Stochastic expression and epigenetic memory at the yeast HO promoter.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Insulator protein Su(Hw) recruits SAGA and Brahma complexes and constitutes part of Origin Recognition Complex-binding sites in the Drosophila genome.Nucleic acids research · 2013Article
- Kinetics and thermodynamics of phenotype: unwinding and rewinding the nucleosome.Journal of molecular biology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
We use chromatin immunoprecipitation assays to show that the Gcn5 histone acetyltransferase in SAGA is required for SWI/SNF association with the HO promoter and that binding of SWI/SNF and SAGA are interdependent. Previous results showed that SWI/SNF binding to HO was Gcn5 independent, but that work used a strain with a mutation in the Ash1 daughter-specific repressor of HO expression. Here, we show that Ash1 functions as a repressor that inhibits SWI/SNF binding and that Gcn5 is required to overcome Ash1 repression in mother cells to allow HO transcription. Thus, Gcn5 facilitates SWI/SNF binding by antagonizing Ash1. Similarly, a mutation in SIN3, like an ash1 mutation, allows both HO expression and SWI/SNF binding in the absence of Gcn5. Although Ash1 has recently been identified in a Sin3-Rpd3 complex, our genetic analysis shows that Ash1 and Sin3 have distinct functions in regulating HO. Analysis of mutant strains shows that SWI/SNF binding and HO expression are correlated and regulated by histone acetylation. The defect in HO expression caused by a mutant SWI/SNF with a Swi2(E834K) substitution can be partially suppressed by ash1 or spt3 mutation or by a gain-of-function V71E substitution in the TATA-binding protein (TBP). Spt3 inhibits TBP binding at HO, and genetic analysis suggests that Spt3 and TBP(V71E) act in the same pathway, distinct from that of Ash1. We have detected SWI/SNF binding at the HO TATA region, and our results suggest that SWI/SNF, either directly or indirectly, facilitates TBP binding at HO.
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.