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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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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]

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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

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.

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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).

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The deubiquitinase USP7 stabilizes Maf proteins to promote myeloma cell survival

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2019-12-16 | PXD016020 | Pride

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