ArticleNature genetics2006
A chromatin-mediated mechanism for specification of conditional transcription factor targets.
Article in Nature genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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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.
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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.
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Who cites it
61 citing papers in PubMed, 94 citations in OpenAlex.
- Rap1 overexpression boosts triterpenoid saponin production in yeast by enhancing precursor supply and heterologous gene expression.Microbial cell factories · 2025Article
- General regulatory factors exert differential effects on nucleosome sliding activity of the ISW1a complex.Biological research · 2024Article
- Telomeres are shorter in wild Saccharomyces cerevisiae isolates than in domesticated ones.Genetics · 2023Article
- Quantitative-enhancer-FACS-seq (QeFS) reveals epistatic interactions among motifs within transcriptional enhancers in developing Drosophila tissue.Genome biology · 2021Article
- Reciprocal stabilization of transcription factor binding integrates two signaling pathways to regulate fission yeast fbp1 transcription.Nucleic acids research · 2021Article
- 3D promoter architecture re-organization during iPSC-derived neuronal cell differentiation implicates target genes for neurodevelopmental disorders.Progress in neurobiology · 2021Article
- Article
- Homotypic cooperativity and collective binding are determinants of bHLH specificity and function.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Defining TP53 pioneering capabilities with competitive nucleosome binding assays.Genome research · 2019Article
- Recruitment and delivery of the fission yeast Rst2 transcription factor via a local genome structure counteracts repression by Tup1-family corepressors.Nucleic acids research · 2017Article
- NicE-seq: high resolution open chromatin profiling.Genome biology · 2017Article
- Systematic dissection of genomic features determining transcription factor binding and enhancer function.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- Local potentiation of stress-responsive genes by upstream noncoding transcription.Nucleic acids research · 2016Article
- Sumoylation controls the timing of Tup1-mediated transcriptional deactivation.Nature communications · 2015Article
- Cis-regulatory mechanisms for robust olfactory sensory neuron class-restricted odorant receptor gene expression in Drosophila.PLoS genetics · 2015Article
- Iron-responsive chromatin remodelling and MAPK signalling enhance adhesion in Candida albicans.Molecular microbiology · 2014Article
- Transcriptional outcome of telomere signalling.Nature reviews. Genetics · 2014Review
- Chromatin accessibility: a window into the genome.Epigenetics & chromatin · 2014Review
- Target analysis by integration of transcriptome and ChIP-seq data with BETA.Nature protocols · 2013Article
1 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
Organisms respond to changes in their environment, and many such responses are initiated at the level of gene transcription. Here, we provide evidence for a previously undiscovered mechanism for directing transcriptional regulators to new binding targets in response to an environmental change. We show that repressor-activator protein 1 (Rap1), a master regulator of yeast metabolism, binds to an expanded target set after glucose depletion despite decreasing protein levels and no evidence of posttranslational modification. Computational analysis predicts that proteins capable of recruiting the chromatin regulator Tup1 act to restrict the binding distribution of Rap1 in the presence of glucose. Deletion of the gene(s) encoding Tup1, recruiters of Tup1 or chromatin regulators recruited by Tup1 cause Rap1 to bind specifically and inappropriately to low-glucose targets. These data, combined with whole-genome measurements of nucleosome occupancy and Tup1 distribution, provide evidence for a mechanism of dynamic target specification that coordinates the genome-wide distribution of intermediate-affinity DNA sequence motifs with chromatin-mediated regulation of accessibility to those sites.
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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.