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Interferon-γ Represses M2 Gene Expression in Human Macrophages by Disassembling Enhancers Bound by the Transcription Factor MAF

ABSTRACT: Interferon-γ Represses M2 Gene Expression in Human Macrophages by Disassembling Enhancers Bound by the Transcription Factor MAF

PROVIDER: PRJNA384911 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5487870.fastq.gz	Fastqsanger.gz
	SRR5487950.fastq.gz	Fastqsanger.gz
	SRR5487960.fastq.gz	Fastqsanger.gz
	SRR5489200.fastq.gz	Fastqsanger.gz
	SRR5489210_1.fastq.gz	Fastqsanger.gz

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Interferon-γ Represses M2 Gene Expression in Human Macrophages by Disassembling Enhancers Bound by the Transcription Factor MAF.

Project description:Mechanisms by which interferon (IFN)-γ activates genes to promote macrophage activation are well studied, but little is known about mechanisms and functions of IFN-γ-mediated gene repression. We used an integrated transcriptomic and epigenomic approach to analyze chromatin accessibility, histone modifications, transcription-factor binding, and gene expression in IFN-γ-primed human macrophages. IFN-γ suppressed basal expression of genes corresponding to an "M2"-like homeostatic and reparative phenotype. IFN-γ repressed genes by suppressing the function of enhancers enriched for binding by transcription factor MAF. Mechanistically, IFN-γ disassembled a subset of enhancers by inducing coordinate suppression of binding by MAF, lineage-determining transcription factors, and chromatin accessibility. Genes associated with MAF-binding enhancers were suppressed in macrophages isolated from rheumatoid-arthritis patients, revealing a disease-associated signature of IFN-γ-mediated repression. These results identify enhancer inactivation and disassembly as a mechanism of IFN-γ-mediated gene repression and reveal that MAF regulates the macrophage enhancer landscape and is suppressed by IFN-γ to augment macrophage activation.

| S-EPMC5568089 | biostudies-literature

IFN-γ Represses M2 Gene Expression in Human Macrophages by Suppressing and Disassembling MAF-binding Enhancers [RNA-seq]

Project description:Mechanisms by which IFN-γ activates genes to promote macrophage activation are well studied, but little is known about mechanisms and functions of IFN-γ-mediated gene repression. We used an integrated transcriptomic and epigenomic approach to analyze chromatin accessibility, histone modifications, transcription factor binding, and gene expression in IFN-γ-primed human macrophages. IFN-γ suppressed basal expression of genes corresponding to an ‘M2’-like homeostatic/reparative phenotype. IFN-γ repressed genes by suppressing the function of enhancers enriched for binding by transcription factor MAF. Mechanistically, IFN-γ ‘disassembled’ a subset of enhancers by inducing coordinate suppression of binding by MAF, lineage-determining transcription factors, and chromatin accessibility. Genes associated with MAF-binding disassembled enhancers were suppressed in rheumatoid arthritis macrophages, revealing a disease-associated ‘negative IFN-γ signature’. These results identify enhancer inactivation and disassembly as a mechanism of IFN-γ-mediated gene repression, and MAF as a regulator of the macrophage enhancer landscape that is suppressed by IFN-γ to augment macrophage activation.

2017-07-01 | GSE98368 | GEO

IFN-γ Represses M2 Gene Expression in Human Macrophages by Suppressing and Disassembling MAF-binding Enhancers [ChIP-seq]

2017-07-01 | GSE98367 | GEO

IFN-γ Represses M2 Gene Expression in Human Macrophages by Suppressing and Disassembling MAF-binding Enhancers [ATAC-seq]

2017-07-01 | GSE98365 | GEO

Interferon-γ Represses M2 Gene Expression in Human Macrophages by Disassembling Enhancers Bound by the Transcription Factor MAF

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

2017-07-01 | GSE98369 | GEO

Transcriptional analysis of transcription factor c-Maf as a molecular switch that controls immune suppression by programming macrophages in lung cancer

Project description:To investigate c-Maf-controlled gene expression, M2-like bone marrow-derived macrophages (BMM) were transfected with c-Maf or control siRNA. Knockdown of c-Maf significantly decreased c-Maf protein and mRNA expression levels. In addition, IL-10 and arginase mRNA levels were significantly decreased while IL-12 was increased. In contrast, ectopic expression of c-Maf in the M1-like BMM significantly upregulated IL-10 and arginase mRNA expression levels while downregulated IL-12 expression level, suggesting an M2-like phenotype. These data indicate that c-Maf may be a critical controller in regulating M2-related gene expression. To further determine which part of the M2 macrophage transcriptomic profile is controlled by c-Maf, we performed microarray analysis using polarized M2-like BMM from WT or c-Maf KO fetal liver chimeric mice. Notably, many M2 genes were differentially regulated by c-Maf. Further real-time PCR (qPCR) analysis confirmed that the mRNA expression levels of IL-12, IL-1β, IL-6, arginase, IL-10, VEGF, TGF-β, IRF-4, and CCR2 were significantly altered in c-Maf-deficient M2 BMM. Since M2-like macrophages have a potent immunosuppressive function on T cell activation, we next determined whether deficiency of c-Maf in M2 BMM would reverse such effect. M2 BMM from WT mice exhibited potent immunosuppressive activity as IFN-γ production from antigen (Ag)-specific CD4 and CD8 T cells was significantly diminished. In contrast, c-Maf deficiency in M2 BMM significantly increased IFN-γ production by CD4 and CD8 T cells compared to WT M2 BMM. These data suggest that c-Maf not only controls many M2-related gene expression but also is critical in regulating M2-like macrophage-mediated T cell immunosuppression.

2020-04-17 | GSE139541 | GEO

WT vs c-Maf KO fetal liver macrophage

Project description:Homozygous disruption of c-Maf led to embryonic lethality and impaired erythroblastic island formation. c-Maf is expressed in the fetal liver macrophages. It suggests that macrophages are responsible for the lethality of c-Maf knock-out embryos. To search downstream genes of c-Maf, we surveyed genes associated with macrophage function by microarray analysis. keywords: c-Maf, macrophage, erythroblastic islands, WT (c-Maf WT) and c-Maf KO (c-Maf KO) fetal liver macrophages were sorted by a FACSAria cell sorter. Total RNAs from those macrophages were prepared using RNeasy Kit. Genes down-regulated in c-Maf KO macrophages were searched by GeneSpring software.

2011-07-06 | E-GEOD-23305 | biostudies-arrayexpress

Maf-S Knockdown Anopheles gambiae: Tiassale

Project description:Transcription factor Maf-S knockdown by dsRNA injection and compared to dsRNA-GFP injected control. Maf-S knockdown was performed to study the affect of xenobiotic stress of the cnc-keap1 pathway.

2017-03-19 | E-MTAB-4042 | biostudies-arrayexpress

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [MAF ChIP-seq]

Project description:We performed genome-wide mapping of MAF binding sites in control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2) stimulation on MAF recruitment to chromatin. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and then E2 or vehicle was added for 1h prior to chromatin immunoprecipitation (ChIP). Samples were generated in triplicate. We report that MAF binding is largely independent of E2

2023-09-15 | GSE210605 | GEO

Identification of MAF controlled genes in breast cancer cells

Project description:To identify relevant genes transcriptionally controlled by MAF in breast cancer, we focused on genes whose expression changed accordingly to MAF transcriptiion factor overexpression in MCF7. We used comparative RNA hybridization (Affymetrix) to this end. Total RNA from parental and MAFshort or long isoform overexpressing MCF7 grown for 48 hours in regular media (see growth protocol) was isolated from in vitro cultured control and MAF expressing MCF7 parental cells. Total RNA was extracted using the TRIzolM-BM-. Plus RNA Purification Kit (Life Technologies).

2014-10-01 | E-GEOD-51231 | biostudies-arrayexpress

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