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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Ogt chromatin recruitment is mediated by TET proteins in mouse ES cells [expression array]

ABSTRACT: O-linked N-acetylglucosamine (O-GlcNAc ) transferase (OGT) activity is essential for embryonic stem (ES) cell viability and mouse development. OGT is present in both cytoplasm and nucleus of different cell types and mediates serine or threonine glycosylation. The Ogt gene locus resides on the X-chromosome and its activity is required for the viability of male ES cells. Using Ogt conditional knock out (KO) ES cells it was shown the failure of establishing stable KO ES clones further suggesting that Ogt activity is required for ES cell self-renewal and pluripotency. For understanding these changes, we performed global gene expression upon silencing of Ogt mediated by esiRNA in mouse Embryonic Stem Cells. Total RNA was extracted from E14 ES cells (derived from Ola129 mice) transiently transfected with Ogt specific and control esiRNA oligos 48 hrs. post-transfection.

ORGANISM(S): Mus musculus

SUBMITTER: Sri Ganesh Jammula

PROVIDER: E-GEOD-39321 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Ogt chromatin recruitment is mediated by TET proteins in mouse ES cells [expression array]

Project description:O-linked N-acetylglucosamine (O-GlcNAc ) transferase (OGT) activity is essential for embryonic stem (ES) cell viability and mouse development. OGT is present in both cytoplasm and nucleus of different cell types and mediates serine or threonine glycosylation. The Ogt gene locus resides on the X-chromosome and its activity is required for the viability of male ES cells. Using Ogt conditional knock out (KO) ES cells it was shown the failure of establishing stable KO ES clones further suggesting that Ogt activity is required for ES cell self-renewal and pluripotency. For understanding these changes, we performed global gene expression upon silencing of Ogt mediated by esiRNA in mouse Embryonic Stem Cells.

2013-01-06 | GSE39321 | GEO

Polycomb proteins link Proliferation with DNA Replication

Project description:Polycomb proteins control proliferation and cellular transformation regulating DNA replication independently of cell cycle checkpoints Total RNA was extracted from MEF cells (derived from Ola129 mice) transiently transfected with Ezh2 specific and control esiRNA oligos 48 hrs. post-transfection.

2014-04-15 | E-GEOD-48520 | biostudies-arrayexpress

Expression changes in Yy1 knock down mouse embryonic stem cells

Project description:We have determined the global gene expression upon loss of function of the Yy1 transcription factor in mouse embryonic stem cells Total RNA was extracted from ES cells transiently transfected with yy1-specific or scrampled-control siRNA oligos 48 hr post-transfection.

2012-01-04 | E-GEOD-31784 | biostudies-arrayexpress

Yy1 activity in mouse embryonic stem cells

Project description:This SuperSeries is composed of the following subset Series: GSE31784: Expression changes in Yy1 knock down mouse embryonic stem cells GSE31785: Yy1 occupancy of mouse ES cell genome Refer to individual Series

2012-01-04 | E-GEOD-31786 | biostudies-arrayexpress

Expression data from ES cells

Project description:TET2 directly interacts with OGT, which is important for the chromatin association of OGT in vivo. Although this specific interaction does not regulate the enzymatic activity of TET2, it facilitates OGT-dependent histone O-GlcNAcylation. Moreover, OGT associates with TET2 at transcription starting sites (TSS). Down-regulation of TET2 reduces the amount of H2B S112 GlcNAc marks in vivo, which are associated with gene transcription regulation. We used microarray to test the function of TET2 on gene expression. Mouse ES cells infected with control knockdown(KD) or TET2 KD virus were treated with puromycin. ES cells were extracted for RNA and hybridization on Affymetrix microarrays.

2012-12-11 | E-GEOD-41721 | biostudies-arrayexpress

HDAC3 requirement for the inflammatory gene expression program in macrophages [gene expression]

Project description:Pan-Hdac inhibitors (HDACi) are endowed with a potent anti-inflammatory activity, but the relative role of each of the eleven Hdac proteins sensitive to HDACi to the inflammatory gene expression program is unknown. Using an integrated genomic approach we found that Hdac3-deficient macrophages are unable to activate almost half of the inflammatory gene expression program when stimulated with lipopolysaccharide (LPS). A large part of the activation defect is due to loss of basal and LPS-inducible expression of IFNb, which in basal cells maintains Stat1 protein levels, and after stimulation acts in an autocrine/paracrine manner to promote a secondary wave of Stat1-dependent gene expression. We show that loss of Hdac3-mediated repression of nuclear receptors leads to hyperacetylation of thousands of genomic sites and associated gene derepression. The upregulation of the constitutively expressed prostaglandin endoperoxide synthase, Ptgs1 (Cox-1), has a causative role in the phenotype, since its chemical inhibition reverts the Ifnb activation defect. These data may have relevance for the use of selective Hdac inhibitors as anti-inflammatory agents. Gene expression profiles for bone marrow-derived macrophages from either HDAC3 +/- (wt) or HDAC3 -/- (KO). Cells were left untreated or challenged with lipopolysaccharide (LPS) for 4hrs. Each genotype-treatment combination was performed in triplicate.

2012-07-08 | E-GEOD-33162 | biostudies-arrayexpress

TET2 and TET3 regulate GlcNAcylation and H3K4 methylation through OGT and SET1/COMPASS

Project description:TET proteins convert 5-methylcytosine to 5-hydroxymethylcytosine, an emerging dynamic epigenetic state of DNA that can influence transcription. Evidence has linked TET1 function to epigenetic repression complexes, yet mechanistic information, especially for the TET2 and TET3 proteins, remains limited. Here, we show a direct interaction of TET2 and TET3 with O-GlcNAc transferase (OGT). OGT does not appear to influence hmC activity, rather TET2 and TET3 promote OGT activity. TET2/3-OGT co-localize on chromatin at active promoters enriched for H3K4me3 and reduction of either TET2/3 or OGT activity results in a direct decrease in H3K4me3 and concomitant decreased transcription. Further, we show that Host Cell Factor 1 (HCF1), a component of the H3K4 methyltransferase SET1/COMPASS complex, is a specific GlcNAcylation target of TET2/3-OGT, and modification of HCF1 is important for the integrity of SET1/COMPASS. Additionally, we find both TET proteins and OGT activity promote binding of the SET1/COMPASS H3K4 methyltransferase, SETD1A, to chromatin. Finally, studies in Tet2 knockout mouse bone marrow tissue extend and support the data as decreases are observed of global GlcNAcylation and also of H3K4me3, notably at several key regulators of haematopoiesis. Together, our results unveil a step-wise model, involving TET-OGT interactions, promotion of GlcNAcylation, and influence on H3K4me3 via SET1/COMPASS, highlighting a novel means by which TETs may induce transcriptional activation. ChIP-Seq experiments were performed on Illumina HiScanSQ sequencer in wild-type HEK293T cells for H3K4me3 histone marks, O-GlcNAc and HCF1, for HT-TET2, HT-TET3 and HT-OGT in HEK293T cells overexpressing those three fusion proteins and in TET2 Kd HEK293T cells for H3K4me3 histone marks. ChIP-Seqs were also performed in mouse bone marrow tissues for H3K4me3 histone marks, O-GlcNAc, endogenous Tet2 and in Tet2 Ko bone marrow tissues for H3K4me3 histone marks.

2013-02-07 | E-GEOD-36620 | biostudies-arrayexpress

Ogt chromatin recruitment is mediated by TET proteins in mouse ES cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-01-06 | E-GEOD-39323 | biostudies-arrayexpress

Ogt chromatin recruitment is mediated by TET proteins in mouse ES cells [ChIP-Seq]

Project description:These data include the genome wide location analysis of Ogt by ChIP of Ogt in mouse ES cells. Precipitation of formaldehyde cross-linked chromatin prepared from mouse ES cell using specific antibody against OGT and IgG as control.

2013-01-06 | E-GEOD-39154 | biostudies-arrayexpress

The Histone Methyltransferase Wbp7 Controls Macrophage Function through GPI Glycolipid Anchor Synthesis. [Expression Profile]

Project description:Histone methyltransferases catalyze site-specific deposition of methyl groups, enabling recruitment of transcriptional regulators. In mammals, trimethylation of lysine 4 in histone H3, a modification localized at the transcription start sites of active genes, is catalyzed by six enzymes (SET1a and SET1b, MLL1M-bM-^@M-^SMLL4) whose specific functions are largely unknown. By using a genomic approach, we found that in macrophages, MLL4 (also known as Wbp7) was required for the expression of Pigp, an essential component of the GPI-GlcNAc transferase, the enzyme catalyzing the first step of glycosylphosphatidylinositol (GPI) anchor synthesis. Impaired Pigp expression in Wbp7-/- macrophages abolished GPI anchor-dependent loading of proteins on the cell membrane. Consistently, loss of GPI-anchored CD14, the coreceptor for lipopolysaccharide (LPS) and other bacterial molecules, markedly attenuated LPS-triggered intracellular signals and gene expression changes. These data link a histone-modifying enzyme to a biosynthetic pathway and indicate a specialized biological role for Wbp7 in macrophage function and antimicrobial response. Gene expression profiles for bone marrow-derived macrophages (BMDM) from either Wbp7+/- (HET) or Wbp7-/- (KO). Cells were left untreated or challenged with lipopolysaccharide (LPS) for 2hrs or 4hrs. Each genotype-treatment combination were performed in triplicate.

2012-04-08 | E-GEOD-30971 | biostudies-arrayexpress

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