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GPS2 cistrome analysis in BMDMs and RAW264.7 cells and epigenome comparison between WT and GPS2-knockout BMDMs.

ABSTRACT: GPS2 binding sites in BMDMs can be localized specially in enhancers (H3K27ac) and promoters (H3K27ac, H3K4me3). Upon GPS2 knock-out in BMDMs, de-repression of certain inflammatory genes occur, as accompanied by increased recruitment of H3K27ac and H3K4me3 marks.

ORGANISM(S): Mus musculus

PROVIDER: GSE66774 | GEO | 2016/06/06

SECONDARY ACCESSION(S): PRJNA277941

REPOSITORIES: GEO

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Expression data of the BMDMs from GPS2 WT and MKO mice

Project description:Obesity is a major risk factor for metabolic disorders like insulin resistance and diabetes. We previously identified GPS2 as a clinical relavant repressor of metaflammation. No animal KO models were used to study its physiological function in vivo. The role of GPS2 in macrophage activation and inflammation is also largely unknown. Here we developed a GPS2 myeloid specific KO mice to study the regulation of GPS2 in macrophage inflammation. We found GPS2 ablation was linked with significant upregulation in inflammation markers in BMDMs from this array.

2016-06-06 | GSE66874 | GEO

Transcriptome comparison between WT and GPS2 liver knockout (LKO) livers and GPS2 NCOR PPARa cistrome and epigenome analysis in livers.

Project description:Obesity-associated lipid overload triggers non-alcoholic fatty liver diseases (NAFLD), which in part may be driven by alterations of regulatory transcription networks and hepatocyte-selective epigenomes. Here we demonstrate that G protein pathway suppressor 2 (GPS2), a subunit of the nuclear receptor corepressor (NCOR)/ histone deacetylase 3 (HDAC3) complex, is a central component of such networks and accelerates the progression of non-alcoholic steatohepatitis (NASH). In hepatocyte-specific Gps2 knockout mice, loss of GPS2 alleviated the development of diet-induced steatosis and fibrosis and caused activation of lipid catabolic genes. By determining differential cistromes, epigenomes and transcriptomes in wild-type, single and double knockout mice, we identified the lipid-sensing nuclear receptor PPARa as a direct target of GPS2. We also provide evidence that in hepatocytes, unlike in macrophages, GPS2 acts in concert with the NCOR subunit of the corepressor complex. By analyzing the liver transcriptomes of human patients, we found that GPS2 expression positively correlated with the expression of NASH/fibrosis signature genes. Collectively, our data suggest that the GPS2-PPARa partnership in hepatocytes may influence the development of NASH/fibrosis in mice and in humans.

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GPS2 sensitizes IL4 pathway via the recruitments of KDM1A

Project description:Here, we systemically investigated the GPS2 corepressor complex function on cyclooxygenase 1 (Ptgs1) in macrophage M2 activation. We found the inflammatory states changed the DNA topology structure along with the histone modification and the gene expression on Ptgs1 locus. GPS2 related NCOR/SMRT corepressor physically bound to Ptgs1 promoter and enhancer, and depletion of all corepressor subunits caused the basal overexpression of Ptgs1 along with the H3K27ac activation. The corepressor subunits display a conserved function on Ptgs1 expression in M2 activation and this regulation is dependent on STAT6 but not through the direct interaction. We find the GPS2 depletion interferences the DNA accessibility on Ptgs1 locus and promotes the enhancer-promoter interaction and the transcriptional process in M2 activation. We further find the GPS2 depletion caused the recruitments of KDM1A, which specifically demethylated the H3K9me2/3 on Ptgs1 locus. In summary, these findings suggest a new paradigm of the corepressor mediated common gene repression in M2 activation and indicate the potential function of the GPS2/NCOR/SMRT function in the tissue homeostasis and wound healing during Th2-mediated immune responses.

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Project description:Transcriptome comparison between WT and GPS2 liver knockout (LKO) livers and GPS2 NCOR PPARa cistrome and epigenome analysis in livers.

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| S-EPMC9043770 | biostudies-literature

A protective strategy against hyperinflammatory responses requiring the non-transcriptional actions of GPS2

2012-03-23 | GSE35197 | GEO

Promoter-specific recruitment of PPARG in adipocytes depends on GPS2-dependent stabilization of histone demethylase KDM4A/JMJD2 [GPS2]

Project description:Timely and selective recruitment of transcription factors to their appropriate DNA-binding sites represents a critical step in regulating gene activation; however the regulatory strategies underlying each factor’s effective recruitment to specific promoter and/or enhancer regions are not fully understood. Here, we identify an unexpected regulatory mechanism by which promoter-specific binding, and therefore function, of PPARG in adipocytes requires G protein Suppressor 2 (GPS2) to prime the local chromatin environment via inhibition of the ubiquitin ligase RNF8 and stabilization of the H3K9 histone demethylase KDM4A/JMJD2. Integration of genome-wide profiling data indicates that the pioneering activity of GPS2/KDM4A is required for PPARG mediated regulation of a specific transcriptional program, including the lipolytic enzymes ATGL and HSL. Hence, our findings reveal that GPS2 exerts a biologically important function in adipose tissue lipid mobilization by directly regulating ubiquitin signaling and indirectly modulating chromatin remodeling to prime selected genes for activation.

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Cop1 wildtype and knock out ChIP-seq for CEBPb, H3K4me3 and H3K27ac in BMDMs

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