Evidence map›Paper›PMID 39747144›Full record

ArticleNature communications2025

Long non-coding RNAs direct the SWI/SNF complex to cell type-specific enhancers.

James A Oo, Timothy Warwick, Katalin Pálfi, Frederike Lam, Francois McNicoll, Cristian Prieto-Garcia, Stefan Günther, Can Cao, Yinuo Zhou, Alexey A Gavrilov and 11 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. 3D Genome Engineering Using CRISPR/dCas Systems.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Review
  5. LINC00607 facilitates endothelial VEGF-A receptor FLT1 splicing.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  6. Article
  7. Direct roles of long non-coding RNAs in transcription activation.Nature structural & molecular biology · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. 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

21 authors.

James A OoGoethe University Frankfurt, Institute for Cardiovascular Physiology, Frankfurt, Germany.
Timothy WarwickGoethe University Frankfurt, Institute for Cardiovascular Physiology, Frankfurt, Germany.ORCID 0000-0002-6804-2931
Katalin PálfiGoethe University Frankfurt, Institute for Cardiovascular Physiology, Frankfurt, Germany.
Frederike LamGoethe University Frankfurt, Institute for Cardiovascular Physiology, Frankfurt, Germany.ORCID 0000-0002-1842-5459
Francois McNicollGoethe University Frankfurt, Institute for Molecular Biosciences, Frankfurt, Germany.
Cristian Prieto-GarciaGoethe University Frankfurt, Institute of Biochemistry II, Faculty of Medicine, Frankfurt, Germany.ORCID 0000-0002-7576-1061
Stefan GüntherMax Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.ORCID 0000-0002-5594-4549
Can CaoGoethe University Frankfurt, Institute for Cardiovascular Physiology, Frankfurt, Germany.ORCID 0000-0001-8559-3535
Yinuo ZhouGoethe University Frankfurt, Institute for Cardiovascular Physiology, Frankfurt, Germany.
Alexey A GavrilovInstitute of Gene Biology, Russian Academy of Sciences, Moscow, Russia.
Sergey V RazinInstitute of Gene Biology, Russian Academy of Sciences, Moscow, Russia.
Alfredo Cabrera-OreficeGoethe University Frankfurt, Institute for Cardiovascular Physiology, Frankfurt, Germany.ORCID 0000-0002-2042-3794
Ilka WittigGoethe University Frankfurt, Institute for Cardiovascular Physiology, Frankfurt, Germany.ORCID 0000-0002-9751-8054
Soni Savai PullamsettiDepartment of Internal Medicine, Justus Liebig University, Giessen, Germany.
Leo KurianGoethe University Frankfurt, Institute for Cardiovascular Physiology, Frankfurt, Germany.ORCID 0000-0001-7466-5169
Ralf GilsbachGoethe University Frankfurt, Institute for Cardiovascular Physiology, Frankfurt, Germany.ORCID 0000-0002-0895-1535
Marcel H SchulzGerman Center of Cardiovascular Research (DZHK), Partner site Rhein/Main, Frankfurt, Germany.ORCID 0000-0002-1252-3656
Ivan DikicCardio-Pulmonary Institute (CPI), Goethe University Frankfurt, Frankfurt, Germany.ORCID 0000-0001-8156-9511
Michaela Müller-McNicollCardio-Pulmonary Institute (CPI), Goethe University Frankfurt, Frankfurt, Germany.ORCID 0000-0002-7174-8310
Ralf P BrandesGoethe University Frankfurt, Institute for Cardiovascular Physiology, Frankfurt, Germany.ORCID 0000-0002-8035-0048
Matthias S LeisegangGoethe University Frankfurt, Institute for Cardiovascular Physiology, Frankfurt, Germany. Leisegang@vrc.uni-frankfurt.de.ORCID 0000-0002-6084-6484

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 390649896Deutsche Forschungsgemeinschaft (German Research Foundation) 403584255Deutsches Zentrum für Herz-Kreislaufforschung (Deutsches Zentrum für Herz-Kreislaufforschung e.V.) 81X2200165
6 · The paper itself

Abstract

The coordination of chromatin remodeling is essential for DNA accessibility and gene expression control. The highly conserved and ubiquitously expressed SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complex plays a central role in cell type- and context-dependent gene expression. Despite the absence of a defined DNA recognition motif, SWI/SNF binds lineage specific enhancers genome-wide where it actively maintains open chromatin state. It does so while retaining the ability to respond dynamically to cellular signals. However, the mechanisms that guide SWI/SNF to specific genomic targets have remained elusive. Here we demonstrate that trans-acting long non-coding RNAs (lncRNAs) direct the SWI/SNF complex to cell type-specific enhancers. SWI/SNF preferentially binds lncRNAs and these predominantly bind DNA targets in trans. Together they localize to enhancers, many of which are cell type-specific. Knockdown of SWI/SNF- and enhancer-bound lncRNAs causes the genome-wide redistribution of SWI/SNF away from enhancers and a concomitant differential expression of spatially connected target genes. These lncRNA-SWI/SNF-enhancer networks support an enhancer hub model of SWI/SNF genomic targeting. Our findings reveal that lncRNAs competitively recruit SWI/SNF, providing a specific and dynamic layer of control over chromatin accessibility, and reinforcing their role in mediating enhancer activity and gene expression.

Indexed as

Chromatin Assembly and DisassemblyChromosomal Proteins, Non-HistoneEnhancer Elements, GeneticRNA, Long NoncodingTranscription FactorsAnimalsChromatinGene Expression RegulationHumansMiceChromatinChromosomal Proteins, Non-HistoneRNA, Long NoncodingSWI-SNF-B chromatin-remodeling complexTranscription Factors

Identifiers

PMID39747144
PMCPMC11695977

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.