Evidence map›Paper›PMID 40217119›Full record

ReviewNature structural & molecular biology2025

A transcription coupling model for how enhancers communicate with their target genes.

Elisabeth Altendorfer, Stefan Mundlos, Andreas Mayer

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature structural & molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Closing 2025, and a look ahead.Nature structural & molecular biology · 2025
    Article
  6. Aberrant Enhancer Regulation, Phase Separation, and Autoimmune Diseases.Clinical reviews in allergy & immunology · 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

3 authors.

Elisabeth AltendorferOtto-Warburg-Laboratory, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Stefan MundlosDevelopment and Disease group, Max Planck Institute for Molecular Genetics, Berlin, Germany.ORCID http://orcid.org/0000-0002-9788-3166
Andreas MayerOtto-Warburg-Laboratory, Max Planck Institute for Molecular Genetics, Berlin, Germany. mayer@molgen.mpg.de.ORCID http://orcid.org/0000-0002-4532-9382

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

How enhancers communicate with their target genes to influence transcription is an unresolved question of fundamental importance. Current models of the mechanism of enhancer-target gene or enhancer-promoter (E-P) communication are transcription-factor-centric and underappreciate major findings, including that enhancers are themselves transcribed by RNA polymerase II, which correlates with enhancer activity. In this Perspective, we posit that enhancer transcription and its products, enhancer RNAs, are elementary components of enhancer-gene communication. Specifically, we discuss the possibility that transcription at enhancers and at their cognate genes are linked and that this coupling is at the basis of how enhancers communicate with their targets. This model of transcriptional coupling between enhancers and their target genes is supported by growing experimental evidence and represents a synthesis of recent key discoveries.

Indexed as

Enhancer Elements, GeneticGene Expression RegulationModels, GeneticTranscription, GeneticAnimalsHumansPromoter Regions, GeneticRNA Polymerase IITranscription FactorsRNA Polymerase IITranscription Factors

Identifiers

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.