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Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE184606 | GEO | 2022/03/21

REPOSITORIES: GEO

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Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [ATAC-seq]

Project description:To determine hemogen function in chromatin accessbility, ATAC Seq was performed in both WT and hemogen KO mouse liver. Loss of hemogen caused generally decresed of chrmoatin accessbility on the hemogen/BRG1 binding promoter and enhancer .

2022-03-21 | GSE184553 | GEO

Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [ChIP-seq]

Project description:To determine hemogen function in regulatory elements, ChIPmentation was performed in both WT and hemogen KO K562 cells and H3K27ac enrichment was significantly reduced at both promoters and enhancers in loss of hemogen. To identify direct targets and the regulatory role of hemogen in murine erythroid gene expression, hemogen and BRG1 ChIP-seq was performed in the WT and hemogen KO E14.5 fetal liver cells. Hemogen was found enriched in GATA1/TAL1 binding motifs and equally bind to the promoter and potential enhancer region. Notably, BRG1 occupancy (95%) was almost completely coincident with hemogen binding sites and loss of hemogen greatly impaired the BRG1 occupancy at both erythroid promoters and enhancers.

2022-03-21 | GSE184605 | GEO

Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [RNA-seq]

Project description:To gain insight into hemogen function during human erythropoiesis, RNA-seq was performed in different type of erythroid cells, such as WT and hemogen KD CD34+ cells, WT and hemogen KD HUDEP2 cells, WT and hemogen KO K562 cells. Notably, depletion of hemogen in these human erythroid cells significantly reduced the expression of genes associated with heme and hemoglobin synthesis, such as ALAS2, HMBS, GYPA, EPOR, and HBB, supporting a positive role of hemogen in erythroid maturation. To further explore hemogen function in mouse embryonic erythropoiesis, RNA-seq was performed in WT and hemogen KO E14.5 fetal liver cells and the data indicated hemogen play a consistently positive role in erythroid maturation-related genes as shown in the human cells, suggested hemogen is conserved activator during the mammalian erythropoiesis.

2022-03-21 | GSE184558 | GEO

Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis

Project description:Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis

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Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [ChIP-seq]

Project description:Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [ChIP-seq]

| PRJNA765350 | ENA

Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [ATAC-seq]

Project description:Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [ATAC-seq]

| PRJNA765025 | ENA

Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [RNA-seq]

Project description:Hemogen /BRG1 cooperativity modulates promoter and enhancer activation during erythropoiesis [RNA-seq]

| PRJNA765029 | ENA

Brg1 modulates enhancer activation in mesoderm lineage commitment.

Project description:The interplay between different levels of gene regulation in modulating developmental transcriptional programs, such as histone modifications and chromatin remodeling, is not well understood. Here, we show that the chromatin remodeling factor Brg1 is required for enhancer activation in mesoderm induction. In an embryonic stem cell-based directed differentiation assay, the absence of Brg1 results in a failure of cardiomyocyte differentiation and broad deregulation of lineage-specific gene expression during mesoderm induction. We find that Brg1 co-localizes with H3K27ac at distal enhancers and is required for robust H3K27 acetylation at distal enhancers that are activated during mesoderm induction. Brg1 is also required to maintain Polycomb-mediated repression of non-mesodermal developmental regulators, suggesting cooperativity between Brg1 and Polycomb complexes. Thus, Brg1 is essential for modulating active and repressive chromatin states during mesoderm lineage commitment, in particular the activation of developmentally important enhancers. These findings demonstrate interplay between chromatin remodeling complexes and histone modifications that, together, ensure robust and broad gene regulation during crucial lineage commitment decisions.

| S-EPMC4392595 | biostudies-literature

Brg1 Modulates Enhancer Activation and Polycomb-mediated Repression in Mesoderm Differentiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-03-01 | GSE45448 | GEO

Neuronal activity-induced BRG1 phosphorylation regulates enhancer activation.

Project description:Neuronal activity-induced enhancers drive gene activation. We demonstrate that BRG1, the core subunit of SWI/SNF-like BAF ATP-dependent chromatin remodeling complexes, regulates neuronal activity-induced enhancers. Upon stimulation, BRG1 is recruited to enhancers in an H3K27Ac-dependent manner. BRG1 regulates enhancer basal activities and inducibility by affecting cohesin binding, enhancer-promoter looping, RNA polymerase II recruitment, and enhancer RNA expression. We identify a serine phosphorylation site in BRG1 that is induced by neuronal stimulations and is sensitive to CaMKII inhibition. BRG1 phosphorylation affects its interaction with several transcription co-factors, including the NuRD repressor complex and cohesin, possibly modulating BRG1-mediated transcription outcomes. Using mice with knockin mutations, we show that non-phosphorylatable BRG1 fails to efficiently induce activity-dependent genes, whereas phosphomimic BRG1 increases enhancer activity and inducibility. These mutant mice display anxiety-like phenotypes and altered responses to stress. Therefore, we reveal a mechanism connecting neuronal signaling to enhancer activities through BRG1 phosphorylation.

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