Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Characterization of genome-wide enhancer-promoter interactions reveals co-expression of interacting genes and modes of higher order chromatin organization

ABSTRACT: Recent epigenomic studies have predicted thousands of potential enhancers in the human genome. However, there has not been systematic characterization of target promoters for these potential enhancers. Using H3K4me2 as a mark for active enhancers, we identified genome-wide enhancer-promoter interactions in human CD4+ T cells. Among the 6,520 long-distance chromatin interactions, we identify 2,067 enhancers that interact with 1,619 promoters and enhance their expression. These enhancers exist in accessible chromatin regions and are associated with various histone modifications and Pol II binding. The promoters with interacting enhancers are expressed at higher levels than those without interacting enhancers and their expression levels are positively correlated with the number of interacting enhancers. Interestingly, interacting promoters are co-expressed in a tissue-specific manner. We also find that chromosomes are organized into multiple levels of interacting domains. Our results define a global view of enhancer-promoter interactions and provide a dataset to further understand mechanisms of enhancer targeting and long-range chromatin organization.

ORGANISM(S): Homo sapiens

PROVIDER: GSE32677 | GEO | 2012/01/24

SECONDARY ACCESSION(S): PRJNA146909

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Characterization of genome-wide enhancer-promoter interactions reveals co-expression of interacting genes and modes of higher order chromatin organization

Project description:Recent epigenomic studies have predicted thousands of potential enhancers in the human genome. However, there has not been systematic characterization of target promoters for these potential enhancers. Using H3K4me2 as a mark for active enhancers, we identified genome-wide enhancer-promoter interactions in human CD4+ T cells. Among the 6,520 long-distance chromatin interactions, we identify 2,067 enhancers that interact with 1,619 promoters and enhance their expression. These enhancers exist in accessible chromatin regions and are associated with various histone modifications and Pol II binding. The promoters with interacting enhancers are expressed at higher levels than those without interacting enhancers and their expression levels are positively correlated with the number of interacting enhancers. Interestingly, interacting promoters are co-expressed in a tissue-specific manner. We also find that chromosomes are organized into multiple levels of interacting domains. Our results define a global view of enhancer-promoter interactions and provide a dataset to further understand mechanisms of enhancer targeting and long-range chromatin organization. Two biological replicates of ChIA-PET (Chromatin Interaction Analysis by Paired-End Tag Sequencing) experiment in CD4+ T cells

2012-01-24 | E-GEOD-32677 | biostudies-arrayexpress

Enhancer-bound LDB1 Regulates a Corticotrope Promoter Pausing Repression Program [ChIP-seq]

Project description:Substantial evidence supports the hypothesis that enhancers are critical regulators of cell type determination, orchestrating both positive and negative transcriptional programs; however, the basic mechanisms by which enhancers orchestrate interactions with cognate promoters during activation and repression events remain incompletely understood. Here we report the required actions of the LIM domain binding protein, LDB1/CLIM2/NLI, interacting with the enhancer binding protein, ASCL1, to mediate looping to target gene promoters and target gene regulation in corticotrope cells. LDB1-mediated enhancer:promoter looping appears to be required for both activation and repression of these target target gene promoter genes. While LDB1-dependend activated genes are regulated at the level of transcriptional initiation, the LDB1-dependent repressed transcription units appear to be regulated primarily at the level of promoter pausing, with LDB1 regulating recruitment of MTA2, a component of the NuRD complex, on these negative enhancers, required for the repressive enhancer function. These results indicate that LDB1-dependent looping events can deliver repressive cargo to cognate promoters to mediate promoter pausing events in a pituitary cell type. ChIP assay followed by high throughput sequencing (ChIP-seq)

2015-02-03 | E-GEOD-64483 | biostudies-arrayexpress

Enhancer-bound LDB1 Regulates a Corticotrope Promoter Pausing Repression Program [GRO-seq]

Project description:Substantial evidence supports the hypothesis that enhancers are critical regulators of cell type determination, orchestrating both positive and negative transcriptional programs; however, the basic mechanisms by which enhancers orchestrate interactions with cognate promoters during activation and repression events remain incompletely understood. Here we report the required actions of the LIM domain binding protein, LDB1/CLIM2/NLI, interacting with the enhancer binding protein, ASCL1, to mediate looping to target gene promoters and target gene regulation in corticotrope cells. LDB1-mediated enhancer:promoter looping appears to be required for both activation and repression of these target target gene promoter genes. While LDB1-dependend activated genes are regulated at the level of transcriptional initiation, the LDB1-dependent repressed transcription units appear to be regulated primarily at the level of promoter pausing, with LDB1 regulating recruitment of MTA2, a component of the NuRD complex, on these negative enhancers, required for the repressive enhancer function. These results indicate that LDB1-dependent looping events can deliver repressive cargo to cognate promoters to mediate promoter pausing events in a pituitary cell type. Global Run On (GRO) assay followed by high throughput sequencing (GRO-seq)

2015-02-03 | E-GEOD-64515 | biostudies-arrayexpress

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

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 | GSE205947 | GEO

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

2023-04-13 | GSE205946 | 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 [ATAC-seq]

2023-04-13 | GSE226300 | GEO

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

2023-04-13 | GSE225294 | 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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