Transient promoter interactions modulate developmental gene activation.

Capture-C chromatin organization distal regulatory elements embryonic stem cell differentiation gene expression genome topology histone modifications temporal dynamics

Journal

Molecular cell
ISSN: 1097-4164
Titre abrégé: Mol Cell
Pays: United States
ID NLM: 9802571

Informations de publication

Date de publication:
23 Oct 2024
Historique:
received: 20 03 2024
revised: 26 08 2024
accepted: 01 10 2024
medline: 31 10 2024
pubmed: 31 10 2024
entrez: 30 10 2024
Statut: aheadofprint

Résumé

Transcriptional induction coincides with the formation of various chromatin topologies. Strong evidence supports that gene activation is accompanied by a general increase in promoter-enhancer interactions. However, it remains unclear how these topological changes are coordinated across time and space during transcriptional activation. Here, we combine chromatin conformation capture with transcription and chromatin profiling during an embryonic stem cell (ESC) differentiation time course to determine how 3D genome restructuring is related to transcriptional transitions. This approach allows us to identify distinct topological alterations that are associated with the magnitude of transcriptional induction. We detect transiently formed interactions and demonstrate by genetic deletions that associated distal regulatory elements (DREs), as well as appropriate formation and disruption of these interactions, can contribute to the transcriptional induction of linked genes. Together, our study links topological dynamics to the magnitude of transcriptional induction and detects an uncharacterized type of transcriptionally important DREs.

Identifiants

pubmed: 39476844
pii: S1097-2765(24)00828-1
doi: 10.1016/j.molcel.2024.10.005
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors declare no competing interests.

Auteurs

Sylvia Mahara (S)

Mechanisms of Genome Control, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, Heidelberg, Germany.

Sonja Prüssing (S)

Mechanisms of Genome Control, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, Heidelberg, Germany.

Valeriia Smialkovska (V)

Mechanisms of Genome Control, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, Heidelberg, Germany.

Samuel Krall (S)

Mechanisms of Genome Control, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, Heidelberg, Germany.

Susannah Holliman (S)

Department of Biochemistry, University of Oxford, Oxford, UK.

Belinda Blum (B)

Mechanisms of Genome Control, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, Heidelberg, Germany.

Victoria Dachtler (V)

Mechanisms of Genome Control, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, Heidelberg, Germany.

Helena Borgers (H)

Mechanisms of Genome Control, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, Heidelberg, Germany.

Etienne Sollier (E)

Division of Cancer Epigenomics, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, Heidelberg, Germany.

Christoph Plass (C)

Division of Cancer Epigenomics, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, Heidelberg, Germany.

Angelika Feldmann (A)

Mechanisms of Genome Control, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, Heidelberg, Germany. Electronic address: angelika.feldmann@dkfz.de.

Classifications MeSH