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Genome-wide maps of Transcriptionalregulation of EGR1 transcription factor in iPAM cells.

ABSTRACT: We applied single-molecule sequencing and high-throughput analysis to analyze the regulation of EGR1 transcription in iPAM cells. By obtaining more than 4 billion base sequences from chromatin immunoprecipitation DNA, we generated a genome-wide chromatin state map of transcriptional regulation of EGR1 transcription factors in iPAM cells. Then, we analyzed the influence of EGR1 transcription regulation on macrophages by analyzing the binding position of EGR1 transcription factor to the genome.

ORGANISM(S): Sus scrofa

PROVIDER: GSE189087 | GEO | 2021/11/20

REPOSITORIES: GEO

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Genome-wide maps of EGR1 binding in mouse frontal cortex

Project description:With anti-EGR1 immunoprecipitated chromatin from mouse prefrontal cortices, we generated EGR1 binding maps with 12, 014 high-confidence peaks. Approximately 81% of EGR1 peaks were within genic regions or nearby promoters, and over 45% EGR1 peaks were in the proximal promoter regions within 1 kb from transcription starting sites.

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EGR1 regulation in human bone marrow stromal cells

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DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells

Project description:To gain insight into the function of DNA-PKcs within immune cells, we performed a quantitative phosphoproteomic screen in T cells to identify first order phosphorylation targets of DNA-PKcs. Results indicate that DNA-PKcs phosphorylates the transcription factor Egr1 (early growth response protein 1) at S301. Expression of Egr1 is induced early upon T cell activation and dictates T cell response by modulating expression of cytokines and key costimulatory molecules. Mutation of serine 301 to alanine via CRISPR-Cas9 resulted in increased proteasomal degradation of Egr1 and a decrease in Egr1-dependent transcription of IL2 (interleukin-2) in activated T cells. Our findings identify DNA-PKcs as a critical intermediary link between T cell activation and T cell fate and a novel phosphosite involved in regulating Egr1 activity.

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Egr1 Recruits Tet1 to Shape the Brain Methylome during Early Postnatal Development

Project description:Early growth response gene-1 (Egr1) is a critical transcription factor involved in many important biological processes, including neuronal plasticity and memory formation. With a rapid increase in expression during the first few weeks after birth, Egr1 controls the selection, maturation and functional integration of newborn neurons. The regulation of Egr1-mediated gene expression has been shown to be under methylation control. However, Egr1 target sites and their epigenetic regulation in the nervous system remains largely unknown. In this study, we performed ChIP-seq for EGR1 in mouse frontal cortex and identified a large number of EGR1 binding sites with their cell-type specific methylation patterns established during postnatal frontal cortex development. More specifically, the CpG dinucleotides within these EGR1 binding sites become hypo-methylated in mature neurons but remain heavily methylated in glia. We further demonstrated that EGR1 recruits a DNA demethylase TET1 to remove DNA methylation at EGR1 binding sites and activate downstream genes. In addition, we found that the frontal cortexes from knockout mice with the loss of Egr1 or Tet1 share strikingly similar profiles in both gene expression and DNA methylation. In summary, our study reveals Egr1 as a key mediator for gene-environment interactions shaping brain methylome together with Tet1 during early postnatal development and provides an important new insight into how early life experience may shape the brain methylome. This SuperSeries is composed of the SubSeries listed below.

2019-07-25 | GSE108768 | GEO

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