Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Increased Enhancer—Promoter Interactions during Developmental Enhancer Activation in Mammals

ABSTRACT: Remote enhancers are thought to interact with their target promoters via physical proximity, yet the importance of this proximity for enhancer function remains unclear. Here, we investigate the 3D conformation of enhancers during mammalian development by generating high-resolution tissue-resolved contact maps for nearly a thousand enhancers with characterized in vivo activities in ten murine embryonic tissues. 61% of developmental enhancers bypass their neighboring genes, which are often marked by promoter CpG methylation. The majority of enhancers display tissue-specific 3D conformations, and both enhancer–promoter and enhancer–enhancer interactions are moderately but consistently increased upon enhancer activation in vivo. Less than 14% of enhancer–promoter interactions form stably across tissues; however, these invariant interactions form in the absence of the enhancer and are likely mediated by adjacent CTCF binding. Our results highlight the general significance of enhancer–promoter physical proximity for developmental gene activation in mammals.

ORGANISM(S): Mus musculus

PROVIDER: GSE217078 | GEO | 2024/01/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The Mediator complex regulates enhancer-promoter interactions [ATAC-seq]

Project description:Enhancer-mediated gene activation generally requires physical proximity between enhancers and their target gene promoters. However, the molecular mechanisms by which interactions between enhancers and promoters are formed are not well understood. Here, we investigate the function of the Mediator complex in the regulation of enhancer-promoter interactions, by combining rapid protein depletion and high-resolution MNase-based chromosome conformation capture approaches. We show that depletion of Mediator leads to reduced enhancer-promoter interaction frequencies, which are associated with a strong decrease in gene expression. In addition, we find increased interactions between CTCF-binding sites upon Mediator depletion. These changes in chromatin architecture are associated with a re-distribution of the Cohesin complex on chromatin and a reduction in Cohesin occupancy specifically at enhancers. Our results indicate that enhancer-promoter interactions are dependent on an interplay between the Mediator and Cohesin complexes and provide new insights into the molecular mechanisms by which communication between enhancers and promoters is regulated.

2023-04-13 | GSE226300 | GEO

The Mediator complex regulates enhancer-promoter interactions [ChIP-seq]

2023-04-13 | GSE225294 | GEO

The Mediator complex regulates enhancer-promoter interactions [Cut&Tag]

2023-04-13 | GSE205905 | GEO

The Mediator complex regulates enhancer-promoter interactions [Capture C]

2023-04-13 | GSE205899 | GEO

The Mediator complex regulates enhancer-promoter interactions [Micro-Capture-C]

2023-04-13 | GSE205946 | GEO

The Mediator complex regulates enhancer-promoter interactions [Tiled-Micro-Capture-C]

2023-04-13 | GSE205947 | GEO

Long-Range Enhancer Interactions Are Prevalent in Mouse Embryonic Stem Cells and Are Reorganized upon Pluripotent State Transition

Project description:Transcriptional enhancers, including super-enhancers (SE), form physical interactions with promoters to regulate cell type-specific gene expression. SE are characterised by high transcription factor occupancy and large domains of active chromatin, and are currently assigned to target promoters using computational predictions. How promoter–SE interactions change upon cell state transitions, and whether transcription factors maintain SE interactions, has not been reported. Here, we used promoter-capture Hi-C to identify promoters in close physical proximity to SE in mouse embryonic stem cells (ESCs). SE form complex, spatial networks in which individual SE contact multiple promoters, and a rewiring of promoter–SE interactions occurs between ESC and EpiSC pluripotent states. Long-range promoter–SE interactions are a hallmark of ESCs and are dependent on the transcription factor NANOG. These results provide new insights into the gene regulatory organization of pluripotent cells and demonstrate the requirement for transcription factors in maintaining a subset of SE interactions.

2018-03-07 | GSE103053 | GEO

Live-cell 3D single-molecule tracking reveals how NuRD modulates enhancer dynamics

Project description:Enhancer-promoter dynamics are crucial for the spatiotemporal control of gene expression, but it remains unclear whether these dynamics are controlled by chromatin regulators, such as the nucleosome remodelling and deacetylase (NuRD) complex. The NuRD complex binds to all active enhancers to modulate transcription and here we use Hi-C experiments to show that it blurs TAD boundaries and increases the proximity of intermediate-range (~1 Mb) genomic sequences and enhancer-promoter interactions. To understand whether NuRD alters the dynamics of 3D genome structure, we developed an approach to segment and extract key biophysical parameters from 3D single-molecule trajectories of the NuRD complex determined using live-cell imaging. Unexpectedly, this revealed that the intact NuRD complex decompacts chromatin structure and makes NuRD-bound enhancers move faster, increasing the overall volume of the nucleus that these key regulatory regions explore. Interestingly, we also uncovered a rare fast-diffusing state of NuRD bound enhancers that exhibits directed motion. The NuRD complex reduces the amount of time that enhancers remain in this fast-diffusing state, which we propose might otherwise re-organise enhancer-promoter proximity.

2023-05-31 | GSE179007 | GEO

MLL-AF4 cooperates with PAF1 and FACT to drive high density enhancer interactions in leukemia

Project description:Aberrant enhancer activation is a key mechanism driving oncogene expression in many cancers. While much is known about the regulation of larger chromosome domains in eukaryotes, the details of enhancer-promoter interactions remain poorly understood. Recent work suggests co-activators like BRD4 and Mediator have little impact on enhancer-promoter interactions. In leukemias controlled by the MLL-AF4 fusion protein, we use the ultra-high resolution technique Micro-Capture-C (MCC) to show that MLL-AF4 binding promotes broad, high-density regions of enhancer-promoter interactions at a subset of key targets. These enhancers are enriched for transcription elongation factors like PAF1C and FACT and loss of these factors abolishes enhancer-promoter contact. This work not only provides a new model for how MLL-AF4 is able to drive high levels of transcription at key genes in leukemia, but also suggests a more general model linking enhancer-promoter crosstalk and transcription elongation.

2023-08-18 | PXD043920 | Pride

Genome-wide nucleosome-resolution map of promoter-centered interactions in human cells corroborates the enhancer-promoter looping model

Project description:The enhancer-promoter looping model, in which enhancers activate their target genes via physical contact, has been the dominant hypothesis in the field for decades. However, a systematic testing of this hypothesis has not been conducted, primarily due to the absence of suitable experimental techniques. In this study, we present a new MNase-based proximity ligation method called MChIP-C, allowing for the measurement of protein-mediated chromatin interactions at single-nucleosome resolution on a genome-wide scale. By applying MChIP-C to study H3K4me3 promoter-centered interactions in K562 cells, we found that it had greatly improved resolution and sensitivity compared to restriction endonuclease-based C-methods. This allowed us to identify EP300 histone acetyltransferase and the SWI/SNF remodelling complex as potential candidates for establishing and/or maintaining enhancer-promoter interactions. Finally, leveraging data from published CRISPRi screens, we found that most functionally-verified enhancers do physically interact with their cognate promoters, supporting the enhancer-promoter looping model.

2023-12-24 | GSE225087 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data