Evidence map›Paper›PMID 41639407›Full record

ArticleNature genetics2026

Transient histone deacetylase inhibition induces cellular memory of gene expression and 3D genome folding.

Flora Paldi, Michael-Florian Szalay, Solène Dufau, Marco Di Stefano, Hadrien Reboul, Daniel Jost, Frédéric Bantignies, Giacomo Cavalli

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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

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  7. Genome-wide absolute quantification of chromatin looping.Nature structural & molecular biology · 2026
    Article
  8. Review
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  14. Review
  15. Article
  16. Recipes and ingredients for deep learning models of 3D genome folding.Current opinion in genetics & development · 2025
    Review
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

8 authors.

Flora PaldiInstitute of Human Genetics (IGH), University of Montpellier, CNRS, Montpellier, France.ORCID http://orcid.org/0000-0002-8776-5879
Michael-Florian Szalay *Institute of Human Genetics (IGH), University of Montpellier, CNRS, Montpellier, France.ORCID http://orcid.org/0000-0002-6310-0610
Solène Dufau *Institute of Human Genetics (IGH), University of Montpellier, CNRS, Montpellier, France.
Marco Di Stefano *Institute of Human Genetics (IGH), University of Montpellier, CNRS, Montpellier, France.ORCID http://orcid.org/0000-0001-6195-4754
Hadrien ReboulInstitute of Human Genetics (IGH), University of Montpellier, CNRS, Montpellier, France.
Daniel JostLaboratoire de Biologie et Modélisation de la Cellule, École Normale Supérieure de Lyon, CNRS UMR 5239, Inserm Université Claude Bernard Lyon, Lyon, France.ORCID http://orcid.org/0000-0002-9877-6864
Frédéric BantigniesInstitute of Human Genetics (IGH), University of Montpellier, CNRS, Montpellier, France.ORCID http://orcid.org/0000-0003-4063-7324
Giacomo CavalliInstitute of Human Genetics (IGH), University of Montpellier, CNRS, Montpellier, France. giacomo.cavalli@igh.cnrs.fr.ORCID http://orcid.org/0000-0003-3709-3469

Funding

European Molecular Biology Organization (EMBO) ATLF 716-2020Human Frontier Science Program (HFSP) LT000111/2021-L
6 · The paper itself

Abstract

Epigenetic memory enables the propagation of gene expression patterns following transient stimuli. Although three-dimensional chromatin organization is emerging as a key regulator of genome function, it is unknown whether it contributes to cellular memory. Here we establish that acute perturbation of the epigenome can induce cellular memory of gene expression in mouse embryonic stem cells. We uncover how a pulse of histone deacetylase inhibition translates to changes in transcription, histone modifications and genome folding. While most epigenomic and transcriptional changes are initially reversed once the perturbation is removed, some loci remain transcriptionally deregulated and genome architecture partially maintains its perturbed conformation. Consequently, a second pulse of transient hyperacetylation induces stronger memory of transcriptional deregulation. Using ultradeep Micro-C, we associate memory of gene expression with repressive Polycomb-mediated chromatin topology. These results demonstrate how cells can record transient stresses in their genome architecture, thereby enabling an enhanced response to subsequent perturbations.

Indexed as

Gene Expression RegulationGenomeHistone Deacetylase InhibitorsAcetylationAnimalsChromatinEpigenesis, GeneticEpigenetic MemoryHistone DeacetylasesHistonesMiceMouse Embryonic Stem CellsTranscription, GeneticChromatinHistone Deacetylase InhibitorsHistone DeacetylasesHistones

Identifiers

PMID41639407
PMCPMC12900649

What OpenQuestion holds

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Registered trials

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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.