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Expression data from intestinal epithelial cells (IECs) [MoGene-1_0-st array]

ABSTRACT: Polycomb group (PcG) proteins are epigenetic silencers whose dysregulation is frequently linked to cancer via mechanisms that remain unclear. Using conditional knock-out mice in a colitis-associated colorectal cancer (CAC) model, we found that Bmi1 and Mel18 are important initiation and maintenance factors during CAC tumorigenesis. Epithelial depletion of both Bmi1 and Mel18, but not either gene alone, significantly reduces tumor growth and multiplicity. We used microarrays to detail the global program of gene expression In DKO, Bmi1ΔIEC, Mel18ΔIEC and WT mice and identified distinct classes of up-regulated genes during this process.

ORGANISM(S): Mus musculus

PROVIDER: GSE57640 | GEO | 2017/11/11

SECONDARY ACCESSION(S): PRJNA247394

REPOSITORIES: GEO

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Expression data from intestinal epithelial cells (IECs) [Mouse430_2 array]

Project description:Polycomb group (PcG) proteins are epigenetic silencers whose dysregulation is frequently linked to cancer via mechanisms that remain unclear. Using conditional knock-out mice in a colitis-associated colorectal cancer (CAC) model, we found that Bmi1 and Mel18 are important initiation and maintenance factors during CAC tumorigenesis. Epithelial depletion of both Bmi1 and Mel18, but not either gene alone, significantly reduces tumor growth and multiplicity. We used microarrays to detail the global program of gene expression In DKO, Bmi1ΔIEC, Mel18ΔIEC and WT mice and identified distinct classes of up-regulated genes during this process.

2017-11-11 | GSE57641 | GEO

Protein interactions within PLEIOHOMEOTIC-repressive complex are critical for its recruitment to Polycomb target genes (Human)

Project description:PcG proteins are critical epigenetic regulators of development. Here we have determined genomic distributions of H3K27me3, BMI1, MEL18, EZH2 and YY1 proteins on chromosomes 8, 11,12 of cultured human NTERA-2 cl.D1 cells by hybridization of ChIP products with tiling microarrays. genomic distributions of H3K27me3, BMI1, MEL18, EZH2 and YY1 proteins on chromosomes 8, 11,12 of cultured human NTERA-2 cl.D1 cells by hybridization of ChIP products with tiling microarrays.

2014-06-07 | E-GEOD-41853 | biostudies-arrayexpress

Protein interactions within PLEIOHOMEOTIC-repressive complex are critical for its recruitment to Polycomb target genes (Human)

2014-06-07 | GSE41853 | GEO

Pilot screen for human PRC1 targeting elements (PTEs)

Project description:PcG proteins are critical epigenetic regulators of development. Here we compared genomic distributions of MEL18 and SUZ12 in NTERA-2 cells to search for sites with unusually high presence of PRC1 compared to that of PRC2 and H3K27me3.

2017-10-25 | GSE101538 | GEO

A cDNA microarray analysis was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells.

Project description:Polycomb group (PcG) proteins including EZH2, SUZ12 ,BMI1,CBX8 and so on, which specifically catalyze trimethylation of histone 3 lysine 27 (H3K27me3), and methylated H3K27 can be recognized by other specific binding proteins to compress chromatin structure, leading to the transcriptional repression of the target genes. To explore a potential functional implication of PcG components in HCC, we stably transfected HepG2 cells with either vectors or constructs expressing shRNA that specifically targets EZH2, SUZ12, BMI1, or CBX8. A cDNA microarray analysis was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells. To obtain a broader understanding of the molecular network of PcG in HCC, the whole genome microarray expression profiling was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells. Comparison of gene expression results from shRNA KDs of EZH2, SUZ12, BMI1 or CBX8 HepG2 cells.

2014-01-16 | E-GEOD-54108 | biostudies-arrayexpress

A cDNA microarray analysis was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells.

2014-01-16 | GSE54108 | GEO

A Region of Human HoxD that Confers Polycomb-Group Responsiveness

Project description:Polycomb group (PcG) proteins are essential for accurate axial body patterning during embryonic development. PcG-mediated repression is conserved in metazoans and is targeted in Drosophila by Polycomb response elements (PREs). Targeting sequences in humans have not been described. While analyzing chromatin architecture in the context of human embryonic stem cell (hESC) differentiation, we discovered a 1.8kb region between HOXD11 and HOXD12 (D11.12) that is associated with PcG proteins, is nuclease hypersensitive, and shows alteration as hESCs differentiate. D11.12 repressed luciferase expression from a reporter construct both before and after differentiation of mesenchymal stem cells into adipocytes. Full repression by D11.12 required a highly conserved region and YY1 binding sites. Repression relied upon PcG proteins Bmi1 and Eed and a YY1-interacting partner, RYBP. We conclude that D11.12 is a Polycomb-dependent regulatory region with similarities to Drosophila PREs, indicating conservation in the mechanisms that target PcG function in mammals and flies. Data contains microarray measurements of the MNase-digested mononucleosomal fragments in hES cells, derived MSCs, osteoblasts and adipocytes. The ChIP-chip data includes Suz12, Bmi1 and H3K27me3 measurements in MSCs and adipocytes.

2010-06-19 | E-GEOD-19046 | biostudies-arrayexpress

Genome wide uH2A localization analysis highlights Bmi1-dependent deposition of the mark at repressed genes.

Project description:Polycomb group (PcG) proteins control organism development by regulating the expression of developmental genes. Transcriptional regulation by PcG proteins is achieved at least partly through the PRC2-mediated methylation on lysine 27 of histone H3 (H3K27) and PRC1-mediated ubiquitylation on lysine 119 of histone H2A (uH2A). As an integral component of PRC1, Bmi1 has been demonstrated to be critical for H2A ubiquitylation. Here we report genome wide localization of the Bmi1-dependent uH2A mark in MEF cells. Gene promoter averaging analysis indicates a peak of uH2A just inside the transcription start site (TSS) of well annotated genes. This peak is enriched at promoters containing the H3K27me3 mark and represents the least expressed genes in WT MEF cells. In addition, peak finding reveals regions of local uH2A enrichment throughout the mouse genome, including almost 700 gene promoters. Genes with promoter peaks of uH2A exhibit lower level expression when compared to genes that do not contain promoter peaks of uH2A. Moreover, we demonstrate that genes with uH2A peaks have increased expression upon Bmi1 knockout. Importantly, local enrichment of uH2A is not limited to regions containing the H3K27me3 mark. We describe the enrichment of H2A ubiquitylation at high density CpG promoters and provide evidence to suggest that DNA methylation may be linked to uH2A at these regions. Thus, our work not only reveals Bmi1-dependent H2A ubiquitylation but also suggests that uH2A targeting in differentiated cells may employ a different mechanism from that in ES cells. Keywords: Epigenetics Examination of uH2A binding in WT and Bmi1 null MEF cells.

2009-05-20 | E-GEOD-15896 | biostudies-arrayexpress

Molecular Dissection of Polycomb Group Protein-mediated Fetal Hemoglobin Repression [RNA-seq]

Project description:The fetal (HbF)-to-adult (HbA) hemoglobin switch is a paradigm for developmental gene expression control with relevance to sickle cell disease and beta-thalassemia. Polycomb repressive complex (PRC) proteins regulate this switch, and an inhibitor of the EED subunit of PRC2 entered clinical trials for fetal hemoglobin activation. Yet, how PcG complexes function in this process, their target genes and relevant subunit composition are unknown. Here, we identified the PRC1 subunit BMI1 as a novel HbF repressor. We uncovered LIN28B, IGF2BP1, and IGF2BP3 as direct BMI1 targets and demonstrate that they account for the BMI1 effects. BMI1 functions as part of the canonical PRC1 (cPRC1) subcomplex as revealed by the physical and functional dissection of BMI1 protein partners. Lastly, we demonstrate that BMI1/cPRC1 acts in concert with the PRC2 to repress HbF through the same target genes. Our study illuminates how PRC silences HbF, highlighting an epigenetic mechanism involved in hemoglobin switching.

2023-03-01 | GSE218232 | GEO

Molecular Dissection of Polycomb Group Protein-mediated Fetal Hemoglobin Repression [CUT&RUN]

2023-03-01 | GSE218231 | GEO

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