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The transcription factor EGR2 is the molecular linchpin connecting STAT6 activation to the stable epigenomic program of alternative macrophage polarization

ABSTRACT: The transcription factor EGR2 is the molecular linchpin connecting STAT6 activation to the stable epigenomic program of alternative macrophage polarization

PROVIDER: PRJNA634372 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11828500.fastq.gz	Fastqsanger.gz
	SRR11828501.fastq.gz	Fastqsanger.gz
	SRR11828502.fastq.gz	Fastqsanger.gz
	SRR11828503.fastq.gz	Fastqsanger.gz
	SRR11828504.fastq.gz	Fastqsanger.gz

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The transcription factor EGR2 is the molecular linchpin connecting STAT6 activation to the stable epigenomic program of alternative macrophage polarization

Project description:Macrophages polarize into functionally distinct subtypes while responding to microenvironmental cues. The identity of proximal transcription factors (TFs) downstream of the polarization signals are known, but their activity is typically transient, failing to explain the long-term, stable epigenomic programs developed. Here, we mapped the early and late epigenomic changes of interleukin-4 (IL-4)-induced alternative macrophage polarization. We identified the TF, Early Growth Response 2 (EGR2), bridging the early-transient and late-stable gene expression program of polarization. EGR2 is a direct target of IL-4-activated STAT6, having broad action indispensable for 77% of the induced gene signature of alternative polarization, including its autoregulation and a robust, downstream TF cascade involving PPARG. Mechanistically, EGR2 binding results in chromatin opening and the recruitment of chromatin remodelers and RNA-polymerase II. Egr2 induction is evolutionarily conserved during alternative polarization of mouse and human macrophages. In the context of tissue resident macrophages, Egr2 expression is most prominent in the lung of a variety of species. Thus, EGR2 is an example of an essential and evolutionarily conserved broad acting factor, linking transient polarization signals to stable epigenomic and transcriptional changes in macrophages.

2020-09-15 | GSE151015 | GEO

The transcription factor EGR2 is the molecular linchpin connecting STAT6 activation to the late, stable epigenomic program of alternative macrophage polarization.

Project description:Macrophages polarize into functionally distinct subtypes while responding to microenvironmental cues. The identity of proximal transcription factors (TFs) downstream from the polarization signals are known, but their activity is typically transient, failing to explain the long-term, stable epigenomic programs developed. Here, we mapped the early and late epigenomic changes of interleukin-4 (IL-4)-induced alternative macrophage polarization. We identified the TF, early growth response 2 (EGR2), bridging the early transient and late stable gene expression program of polarization. EGR2 is a direct target of IL-4-activated STAT6, having broad action indispensable for 77% of the induced gene signature of alternative polarization, including its autoregulation and a robust, downstream TF cascade involving PPARG. Mechanistically, EGR2 binding results in chromatin opening and the recruitment of chromatin remodelers and RNA polymerase II. Egr2 induction is evolutionarily conserved during alternative polarization of mouse and human macrophages. In the context of tissue resident macrophages, Egr2 expression is most prominent in the lung of a variety of species. Thus, EGR2 is an example of an essential and evolutionarily conserved broad acting factor, linking transient polarization signals to stable epigenomic and transcriptional changes in macrophages.

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Genetic interrogation of STAT6-mediated macrophage polarization to tumorigenesis in a sterile, penetrant, autochthonous cancer model

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Genome-wide analysis of STAT6 target genes in IL-4 treated human cord blood CD4+ cells

Project description:STAT6 is a major transcription factor driving the polarization of Th2 cells in response to cytokine IL-4. Here we have analyzed on a genome wide level the STAT6 mediated gene expression after IL-4 induction in naive human CD4+ T cells. RNAi mediated STAT6 knockdown was used to reveal the genes specifically regulated by STAT6. Total RNA from STAT6 siRNA treated cord blood CD4+ T cells 12, 24, 48 or 72 hours after culturing the cells in activating (antiCD3+antiCD28) plus or minus IL-4 conditions was compared to total RNA from nonspecific control siRNA treated cells. All together 18 samples were analyzed and 3 biological replicates of the culture were performed for a total of 54 samples.

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RNA-seq of FR4+Egr2+, FR4+Egr2-, FR4-Egr2-, FR4+Egr2-/-Egr3-/- and FR4-Egr2-/-Egr3-/- CD4 T cells

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