ArticleGenome research2022
A systematic genome-wide account of binding sites for the model transcription factor Gcn4.
Article in Genome research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 14 citations in OpenAlex.
- Nucleosomes and IDRs suppress promiscuous GCN4 binding on minichromosomes.Nature structural & molecular biology · 2026Article
- BPabZIP, a new bZIP protein motif that promotes binding near, and displacement of, nucleosomes.bioRxiv : the preprint server for biology · 2026Article
- Sir proteins impede, but do not prevent, access to silent chromatin in living Saccharomyces cerevisiae.Scientific reports · 2026Article
- A dual reporter system for intracellular and extracellular amino acid sensing in budding yeast.Molecular biology of the cell · 2025Article
- The calcineurin-responsive transcription factor Crz1 regulates the expression of CMK2 via a sole CDRE site in its promoter in budding yeast.Scientific reports · 2025Article
- The yeast genome is globally accessible in living cells.Nature structural & molecular biology · 2025Article
- Loss of Gst1 enhances resistance to MMS by reprogramming the transcription of DNA damage response genes in a Rad53-dependent manner in Candida albicans.Cell communication and signaling : CCS · 2024Article
- Bayesian inference of sample-specific coexpression networks.Genome research · 2024Article
- Multilevel Regulation of Membrane Proteins in Response to Metal and Metalloid Stress: A Lesson from Yeast.International journal of molecular sciences · 2024Review
- Bayesian Optimized sample-specific Networks Obtained By Omics data (BONOBO).bioRxiv : the preprint server for biology · 2023Article
- Zinc cluster transcription factors frequently activate target genes using a non-canonical half-site binding mode.Nucleic acids research · 2023Article
- Double DAP-seq uncovered synergistic DNA binding of interacting bZIP transcription factors.Nature communications · 2023Article
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
Sequence-specific DNA-binding transcription factors are central to gene regulation. They are often associated with consensus binding sites that predict far more genomic sites than are bound in vivo. One explanation is that most sites are blocked by nucleosomes, such that only sites in nucleosome-depleted regulatory regions are bound. We compared the binding of the yeast transcription factor Gcn4 in vivo using published ChIP-seq data (546 sites) and in vitro, using a modified SELEX method ("G-SELEX"), which utilizes short genomic DNA fragments to quantify binding at all sites. We confirm that Gcn4 binds strongly to an AP-1-like sequence (TGACTCA) and weakly to half-sites. However, Gcn4 binds only some of the 1078 exact matches to this sequence, even in vitro. We show that there are only 166 copies of the high-affinity RTGACTCAY site (exact match) in the yeast genome, all occupied in vivo, largely independently of whether they are located in nucleosome-depleted or nucleosomal regions. Generally, RTGACTCAR/YTGACTCAY sites are bound much more weakly and YTGACTCAR sites are unbound, with biological implications for determining induction levels. We conclude that, to a first approximation, Gcn4 binding can be predicted using the high-affinity site, without reference to chromatin structure. We propose that transcription factor binding sites should be defined more precisely using quantitative data, allowing more accurate genome-wide prediction of binding sites and greater insight into gene regulation.
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.