Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription Factor GATA2 Promotes Chromatin Remodeling at the Super-Enhancers of the Key Mast Cell Identity Genes and Primes Enhancers to Respond to Antigenic Stimulation [ATAC-seq]

ABSTRACT: Mast cells are critical effectors in causing allergic inflammation and in protecting against certain parasitic infections. We previously demonstrated that transcription factors GATA2 and MITF are the mast cell lineage-determining factors (LDTFs). However, it is unclear whether these LDTFs play a role in regulating chromatin accessibility at the enhancer regions. In this study, we demonstrate that GATA2 promotes chromatin accessibility at the super-enhancers of mast cell identity genes and primes both the typical and super-enhancers at the genes that respond to antigenic stimulation. We found that the number and densities of GATA2, but not MITF, -bound sites at the super-enhancers were several folds higher than that at the typical enhancers. Our study reveals that GATA2 promotes robust gene transcription to maintain mast cell identity and respond to antigenic stimulation simply by binding to a larger number of GATA2 binding sites available at the super-enhancers of the key mast cell genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE145542 | GEO | 2020/11/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcription Factor GATA2 Promotes Chromatin Remodeling at the Super-Enhancers of the Key Mast Cell Identity Genes and Primes Enhancers to Respond to Antigenic Stimulation [RNA-seq]

Project description:Mast cells are critical effectors in causing allergic inflammation and in protecting against certain parasitic infections. We previously demonstrated that transcription factors GATA2 and MITF are the mast cell lineage-determining factors (LDTFs). However, it is unclear whether these LDTFs play a role in regulating chromatin accessibility at the enhancer regions. In this study, we demonstrate that GATA2 promotes chromatin accessibility at the super-enhancers of mast cell identity genes and primes both the typical and super-enhancers at the genes that respond to antigenic stimulation. We found that the number and densities of GATA2, but not MITF, -bound sites at the super-enhancers were several folds higher than that at the typical enhancers. Our study reveals that GATA2 promotes robust gene transcription to maintain mast cell identity and respond to antigenic stimulation simply by binding to a larger number of GATA2 binding sites available at the super-enhancers of the key mast cell genes.

2020-11-25 | GSE145611 | GEO

Transcription Factor GATA2 Promotes Chromatin Remodeling at the Super-Enhancers of the Key Mast Cell Identity Genes and Primes Enhancers to Respond to Antigenic Stimulation [ChIP-seq]

2020-11-25 | GSE145544 | GEO

Transcription Factor GATA2 Promotes Chromatin Remodeling at the Super-Enhancers of the Key Mast Cell Identity Genes and Primes Enhancers to Respond to Antigenic Stimulation

Project description:Transcription Factor GATA2 Promotes Chromatin Remodeling at the Super-Enhancers of the Key Mast Cell Identity Genes and Primes Enhancers to Respond to Antigenic Stimulation

| PRJNA607740 | ENA

Transcription Factor GATA2 Promotes Chromatin Remodeling at the Super-Enhancers of the Key Mast Cell Identity Genes and Primes Enhancers to Respond to Antigenic Stimulation [RNA-seq]

Project description:Transcription Factor GATA2 Promotes Chromatin Remodeling at the Super-Enhancers of the Key Mast Cell Identity Genes and Primes Enhancers to Respond to Antigenic Stimulation [RNA-seq]

| PRJNA607738 | ENA

Transcription Factor GATA2 Promotes Chromatin Remodeling at the Super-Enhancers of the Key Mast Cell Identity Genes and Primes Enhancers to Respond to Antigenic Stimulation [ChIP-seq]

| PRJNA607532 | ENA

Transcription Factor GATA2 Promotes Chromatin Remodeling at the Super-Enhancers of the Key Mast Cell Identity Genes and Primes Enhancers to Respond to Antigenic Stimulation [ATAC-seq]

| PRJNA607533 | ENA

Master Transcription Factors and Mediator Establish Super-Enhancers at Key Cell Identity Genes [ChIP-Seq]

Project description:The master transcription factors Oct4, Sox2 and Nanog bind enhancer elements and recruit the Mediator co-activator to activate much of the gene expression program of embryonic stem cells (ESCs). We report here that the ESC master transcription factors and Mediator form “super-enhancers” at most genes known to control the pluripotent state, including those encoding the master transcription factors themselves. These super-enhancers consist of extraordinarily large genomic domains occupied by exceptional amounts of Oct4, Sox2, Nanog, Klf4, Esrrb and Mediator. Super-enhancers stimulate considerably higher transcription than typical enhancers in vivo and in reporter vectors. Reduced levels of Oct4 or Mediator cause preferential loss of expression of super-enhancer-associated genes relative to other genes, suggesting how changes in gene expression programs might be accomplished during development. In other more differentiated cells, super-enhancers containing cell-type-specific master transcription factors are also found at genes that define cell identity. These results implicate super-enhancers in the control of mammalian cell identity and differentiation. ChIP-Seq and controls associated with Super-Enhancers in murine cell types

2013-02-13 | E-GEOD-44286 | biostudies-arrayexpress

Master Transcription Factors and Mediator Establish Super-Enhancers at Key Cell Identity Genes [gene expression]

Project description:The master transcription factors Oct4, Sox2 and Nanog bind enhancer elements and recruit the Mediator co-activator to activate much of the gene expression program of embryonic stem cells (ESCs). We report here that the ESC master transcription factors and Mediator form M-bM-^@M-^\super-enhancersM-bM-^@M-^] at most genes known to control the pluripotent state, including those encoding the master transcription factors themselves. These super-enhancers consist of extraordinarily large genomic domains occupied by exceptional amounts of Oct4, Sox2, Nanog, Klf4, Esrrb and Mediator. Super-enhancers stimulate considerably higher transcription than typical enhancers in vivo and in reporter vectors. Reduced levels of Oct4 or Mediator cause preferential loss of expression of super-enhancer-associated genes relative to other genes, suggesting how changes in gene expression programs might be accomplished during development. In other more differentiated cells, super-enhancers containing cell-type-specific master transcription factors are also found at genes that define cell identity. These results implicate super-enhancers in the control of mammalian cell identity and differentiation. Time-course of gene expression following shRNA knockdown of Oct4 and Med12.

2013-02-13 | E-GEOD-44287 | biostudies-arrayexpress

Master Transcription Factors and Mediator Establish Super-Enhancers at Key Cell Identity Genes

Project description:The master transcription factors Oct4, Sox2 and Nanog bind enhancer elements and recruit the Mediator co-activator to activate much of the gene expression program of embryonic stem cells (ESCs). We report here that these ESC master transcription factors and Mediator form M-bM-^@M-^\super-enhancersM-bM-^@M-^] at most genes that are known to control the pluripotent state, including those encoding the master transcription factors themselves. These super-enhancers consist of extraordinarily large genomic domains occupied by exceptional amounts of Oct4 and Mediator. Super-enhancers stimulate considerably higher transcription than typical enhancers in reporter vectors. ESC differentiation causes preferential loss of expression of super-enhancer -associated genes. Super-enhancers are also found at key cell identity genes in differentiated cells. These results implicate super-enhancers in the control of mammalian cell identity and differentiation and suggest that these elements might generally be used to identify genes that control cell-type specific gene expression programs in many mammalian cells. ChIP-Seq and RNA-seq of Med1 in ZHBTc4 ES during treatment with doxycycline. ChIP-Seq data of Med1 in 38B9 pro-B cells.

2013-01-02 | E-GEOD-42474 | biostudies-arrayexpress

Striatal genes regulated by super-enhancers and displaying low paused RNAPII are preferentially down-regulated in Huntington’s disease [ChIP-seq]

Project description:Huntington neurodegenerative disease (HD) is associated with extensive down-regulation of neuronal genes. We show preferential down-regulation of super-enhancer-regulated neuronal function genes in the striatum of HD mice. Striatal super-enhancers display extensive H3K27 acetylation within gene bodies and drive transcription characterized by low levels of paused RNAPII. Down-regulation of gene expression is associated with diminished H3K27 acetylation and RNAPII recruitment. Striatal super-enhancers are enriched in binding motifs for Gata transcription factors, such as Gata2 regulating striatal identity genes. Thus, enhancer topography and transcription dynamics are major parameters determining the propensity of a gene to be deregulated in a neurodegenerative disease. Examination of H3k27ac and RNA pol II in Striatum by deep sequencing

2015-04-01 | E-GEOD-59570 | biostudies-arrayexpress

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