Evidence map›Paper›PMID 42538372›Full record

ArticleNature genetics2026

Cumulative transcription factor binding and p300-mediated histone acetylation drive enhancer activation frequency.

Valentina Baderna, Guido Barzaghi, Rozemarijn Kleinendorst, Kasit Chatsirisupachai, Laura Moniot-Perron, Colm Doyle, Meike Schopp, Tino Hochepied, Claude Libert, Duncan T Odom and 2 more

Abstract read
In one paragraph

Article in Nature genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Valentina Baderna *Genome Biology Unit, EMBL Heidelberg, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-2053-3926
Guido Barzaghi *Genome Biology Unit, EMBL Heidelberg, Heidelberg, Germany.ORCID http://orcid.org/0000-0001-6066-3920
Rozemarijn KleinendorstGenome Biology Unit, EMBL Heidelberg, Heidelberg, Germany.
Kasit ChatsirisupachaiGenome Biology Unit, EMBL Heidelberg, Heidelberg, Germany.ORCID http://orcid.org/0000-0001-9446-6714
Laura Moniot-PerronGenome Biology Unit, EMBL Heidelberg, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-6224-6925
Colm DoyleGenome Biology Unit, EMBL Heidelberg, Heidelberg, Germany.
Meike SchoppGerman Cancer Research Center (DKFZ), Division of Regulatory Genomics and Cancer Evolution, Heidelberg, Germany.
Tino HochepiedVIB Center for Inflammation Research, Ghent, Belgium.
Claude LibertVIB Center for Inflammation Research, Ghent, Belgium.ORCID http://orcid.org/0000-0001-6408-036X
Duncan T OdomGerman Cancer Research Center (DKFZ), Division of Regulatory Genomics and Cancer Evolution, Heidelberg, Germany.ORCID http://orcid.org/0000-0001-6201-5599
Judith B ZauggStructural and Computational Biology Unit, EMBL Heidelberg, Heidelberg, Germany. judith.zaugg@embl.de.
Arnaud R KrebsGenome Biology Unit, EMBL Heidelberg, Heidelberg, Germany. arnaud.krebs@embl.de.ORCID http://orcid.org/0000-0001-7999-6127

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) KR 5247/1-2, KR 5247/1-3
6 · The paper itself

Abstract

In eukaryotes, transcription factors (TFs) must continuously compete with nucleosomes to access their binding sites, leading to cell-to-cell variability in chromatin accessibility at regulatory regions. Although critical to understand enhancer function in transcription, the mechanisms that define how frequently an enhancer is active in a cell population remain unclear. Here we used single-molecule footprinting to quantify the frequency at which chromatin is accessible at enhancers in response to TF perturbations and changes in their chromatin environment. We find that, individually, most TFs open chromatin in a small fraction of cells, and that cumulative TF binding controls enhancer activation frequency. Moreover, testing the functionality of hundreds of enhancers when inserted at an ectopic genomic location indicates that p300 activity is required for their full activation. Our data support a model in which enhancer activation frequency depends on the cumulative function of multiple TFs and is modulated by p300 activity.

Indexed as

E1A-Associated p300 ProteinEnhancer Elements, GeneticHistonesp300-CBP Transcription FactorsTranscription FactorsAcetylationAnimalsBinding SitesChromatinHumansNucleosomesProtein BindingTranscriptional ActivationChromatinE1A-Associated p300 ProteinHistonesNucleosomesp300-CBP Transcription FactorsTranscription Factors

Identifiers

PMID42538372
PMCPMC13447113

What OpenQuestion holds

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Registered trials

None linked

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.