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Epigenome analysis of liver tissues from Pemt-/- and Pemt+/+ under high fat-high sucrose (HFHS) diet

ABSTRACT: Genome wide DNA methylation profiling of liver tissues from Pemt-/- and Pemt+/+ under HFHS diets. Pemt-/- and Pemt+/+ mice were fed HFHS from 5 to 25 weeks of age and liver tissues were obtained at 25 weeks. Bisulphite converted DNAs were enriched with EpiXplore Methylation DNA Enrichment Kit (Clontech). Genomic DNA libraries was prepared by TruSeq ChIP Sample Preparation Kit.

ORGANISM(S): Mus musculus

SUBMITTER: Jun Wada

PROVIDER: E-GEOD-67791 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from liver samples of Pemt-/- and Pemt+/+ mice under high fat-high-sucrose (HFHS) diet

Project description:We used microarrays to detail the global programme of gene expression in the liver of Pemt-/- and Pemt+/+ under HFHS diets. Liver sample of Pemt-/- and Pemt+/+ mice under HFHS for 1, 2, 3, 4 weeks were used for RNA extraction and hybridization on Affymetrix microarrays. Genes in liver of Pemt-/- mice, successively suppressed compared with Pemt+/+ mice, were obtained.

2015-04-14 | E-GEOD-67792 | biostudies-arrayexpress

Opposing roles for the lncRNA Haunt and its genomic locus in regulating HOXA gene activation during embryonic stem cell differentiation

Project description:Long noncoding RNAs (lncRNAs) have been implicated in controlling various aspects of embryonic stem cell (ESC) biology, although the functions of specific lncRNAs, and the molecular mechanisms through which they act, remain unclear. Here, we demonstrate discrete and opposing roles for the lncRNA transcript Haunt and its genomic locus in regulating the HOXA gene cluster during ESC differentiation. Reducing or enhancing Haunt expression, with minimal disruption of the Haunt locus, led to up- or down-regulation of HOXA genes, respectively. In contrast, increasingly large genomic deletions within the Haunt locus attenuated HOXA activation. The Haunt DNA locus contains potential enhancers of HOXA activation, whereas Haunt RNA acts to prevent aberrant HOXA expression. This work reveals a multi-faceted model of lncRNA-mediated transcriptional regulation of the HOXA cluster, with distinct roles for a lncRNA transcript and its genomic locus, while illustrating the power of rapid CRISPR/Cas9-based genome editing for assigning lncRNA functions. All RNA-seq(s) were designed to reveal the differentially expressed genes among different stages of ESCs differentiation, or differentially expressed genes between wild-type or Haunt or HOXA mutant cells during RA-induced differentiation. All ChIRP-Seq were used to reveal the DNA or RNA targets of Haunt before or after RA treatment.

2015-04-20 | E-GEOD-58514 | biostudies-arrayexpress

Epigenome analysis of liver tissues from Pemt-/- and Pemt+/+ under high fat-high sucrose (HFHS) diet

Project description:Genome wide DNA methylation profiling of liver tissues from Pemt-/- and Pemt+/+ under HFHS diets.

2015-04-14 | GSE67791 | GEO

Expression data from liver samples of Pemt-/- and Pemt+/+ mice under high fat-high-sucrose (HFHS) diet

Project description:We used microarrays to detail the global programme of gene expression in the liver of Pemt-/- and Pemt+/+ under HFHS diets.

2015-04-14 | GSE67792 | GEO

ChIP-Seq for Nkx3-1 in whole mouse prostate

Project description:We report the genome-wide binding sites of the NK homeodomain transcription factor, Nkx3-1, in mouse prostate. Three different mouse genotypes were used: Nkx3-1 wild-type (WT), Nkx3-1 heterozygote (HET), and Nkx3-1 knock-out (KO). Two biological replicates were performed for WT and HET, and one replicate for KO. The mice used were a recombinant inbred C57BL6/J x 129 strain. The KO dataset was used as a control in lieu of an IgG. Examination of Nkx3-1 binding sites in Nkx3-1+/+ (WT), +/- (HET) and -/- (KO) mouse prostates

2012-04-09 | E-GEOD-35971 | biostudies-arrayexpress

Remodelling of the acetylproteome by SIRT3 manipulation fails to affect insulin secretion or beta-cell metabolism in the absence of over nutrition

Project description:From Peterson et. al. 2018: SIRT3 is an NAD+-dependent mitochondrial protein deacetylase purported to influence metabolism through post-translational modification of metabolic enzymes. Fuel-stimulated insulin secretion, which involves mitochondrial metabolism, could be susceptible to SIRT3-mediated effects. We used CRISPR/Cas9 technology to manipulate SIRT3 expression in b-cells, resulting in wide-spread, SIRT3dependent changes in acetylation of key metabolic enzymes, but with no appreciable changes in glucose- or pyruvate-stimulated insulin secretion, or in metabolomic profile during glucose stimulation. Moreover, these broad changes in the SIRT3-targeted acetylproteome did not affect responses to nutritional or ER stress conditions. We also studied mice with global SIRT3 knockout fed either standard chow (STD) or high- fat/high-sucrose (HFHS) diets. Only when chronically fed a HFHS diet do SIRT3 KO animals exhibit a modest reduction in insulin secretion. We conclude that broad changes in mitochondrial protein acetylation in response to manipulation of SIRT3 are not sufficient to cause changes in islet function or metabolism.

2018-06-21 | PXD009509 | Pride

Comparison of genome-wide DNA methylation in MEFs derived from wildtype or estrogen receptor beta null mice using reduced representation bisulfite sequencing

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2016-02-22 | E-GEOD-72230 | biostudies-arrayexpress

H3K27me3 is not required for recruitment of Polycomb repressor complex 1 to target loci in mouse embryonic stem cells

Project description:The established hierarchical model explaining co-occupancy of Polycomb repressor complexes 1 and 2 (PRC 1 and 2) at target loci proposes that the chromodomain of the polycomb protein, a core PRC1 subunit, recognises the H3K27me3 histone modification catalysed by PRC2. We used chromatin immunoprecipitation to analyse PRC1 occupancy at target loci in Eed-/- mouse embryonic stem cells (ESCs) that lack H3K27me3. Occupancy of the core PRC1 proteins Ring1B and Mel18 was strongly reduced, consistent with the hierarchical model. However, levels of H2A ubiquitylation (H2AK119u1), the histone modification catalysed by PRC1, were similar to wild-type cells, suggesting PRC1 recruitment is independent of H3K27me3. ChIP-sequencing analysis of Ring1B occupancy genome wide substantiated this conclusion, demonstrating significant Ring1B levels at polycomb target loci in Eed-/- ESCs. Thus PRC1 and PRC2 are recruited independently to sites that they co-occupy. We conclude that the primary function of H3K27me3 is to increase the residency of PRC1 at target loci and thereby to contribute to the stability of PRC1 mediated silencing. Examination of Ring1B binding in WT, Eed ko and Input of ESCs Examination of CBX7 in WT and Eed ko of ESCs

2011-11-30 | E-GEOD-23716 | biostudies-arrayexpress

Liver samples of Pemt-/- and Pemt+/+ mice under high fat-high-sucrose (HFHS) diet

Project description:Liver samples of Pemt-/- and Pemt+/+ mice under high fat-high-sucrose (HFHS) diet

| PRJNA280947 | ENA

Genome-wide analyses reveal the extent of opportunistic STAT5 binding that does not yield transcriptional activation of neighboring genes.

Project description:Signal Transducers and Activators of Transcription (STAT) 5A/B regulate cytokine-inducible genes upon binding to GAS motifs. It is not known what percentage of genes with GAS motifs bind to and are regulated by STAT5. Moreover, it is not clear whether genome-wide STAT5 binding is modulated by its concentration. To clarify these issues we established genome-wide STAT5 binding upon growth hormone (GH) stimulation of wild type mouse embryonic fibroblasts (MEFs) and MEFs overexpressing STAT5A more than 20-fold. Upon GH stimulation 23,827 and 111,939 STAT5A binding sites were detected in wild type and STAT5A overexpressing MEFs, respectively. 13,278 and 71,561 peaks contained at least one GAS motif. 1,586 and 8,613 binding sites were located within 2.5 kbp of promoter sequences, respectively. Stringent filtering revealed 78 genes in which the promoter/upstream region (-10kbp to +0.5kbp) was recognized by STAT5 both in wt and STAT5 overexpressing MEFs and 347 genes that bound STAT5 only in overexpressing cells. Genome-wide expression analyses identified that the majority of STAT5-bound genes was not under GH control. Up to 40% of STAT5-bound genes were not expressed. For the first time we demonstrate the magnitude of opportunistic genomic STAT5 binding that does not translate into transcriptional activation of neighboring genes. Genome-wide mapping of STAT5 binding in MEF cells (WT, KO; Stat5-/- and overexpression; STAT5A-Stat5-/-) upon growth hormone induction

2012-01-12 | E-GEOD-34986 | biostudies-arrayexpress

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