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Epigenetic marks and factors binding to chromatin in mouse embryonic stem cells

ABSTRACT: The goal is to profile several histone modifications and hnRNP L in untreated or Adriamycin-treated mouse embryonic stem cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE62864 | GEO | 2015/06/05

SECONDARY ACCESSION(S): PRJNA265860

REPOSITORIES: GEO

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Epigenetic marks and factors binding to chromatin in mouse embryonic stem cells

Project description:The goal is to profile several histone modifications and hnRNP L in untreated or Adriamycin-treated mouse embryonic stem cells. Fifty million of R1E mES cells were untreated or treated with 0.5 uM Adriamycin for 8 hours. Fixed cells were subject to ChIP-seq assay.

2015-06-05 | E-GEOD-62864 | biostudies-arrayexpress

Regulatory RNA Apela Is a Component of a Negative Feedback Loop Regulating p53-Mediated Apoptosis in Embryonic Stem Cells (III)

Project description:The goal is to identify RNAs that bind to Hnrnpl (hnRNP L) using RNA immunoprecipitation (RIP) assay. p53+/+ mES cells and p53-/- mES cells were untreated or treated with 0.5 uM Adriamycin for 8 hours. RNA immunoprecipitation was performed using Hnrnpl antibody (Bethyl, Cat#: A311-423A). Total RNA was extracted and subject to RNAseq.

2015-06-05 | E-GEOD-62378 | biostudies-arrayexpress

Regulatory RNA Apela Is a Component of a Negative Feedback Loop Regulating p53-Mediated Apoptosis in Embryonic Stem Cells (II)

Project description:The goal is to identify regulatory RNAs that regulate the p53 signaling pathway in embryonic stem (ES) cells. p53+/+ mES cells and p53-/- mES cells were untreated or treated with 0.5 uM Adriamycin for 8 hours. Total RNA was extracted and subject to RNAseq.

2015-06-05 | E-GEOD-60843 | biostudies-arrayexpress

Combinatorial role of two paralogous splicing factors, hnRNP L and L-like, in multiple-exon regulation of CD45 alternative splicing

Project description:The goal of this study was to investigate the role of hnRNP L-like in alternative pre-mRNA splicing in human B-cells through an RNA-Seq approach. RNA-Seq was performed in DG75 cell line with over expression of hnRNP L-like or GFP as control.

2012-03-28 | E-GEOD-33013 | biostudies-arrayexpress

Transcription factors, coregulators, and epigenetic marks are linearly correlated and highly redundant.

Project description:The DNA microstates that regulate transcription include sequence-specific transcription factors (TFs), coregulatory complexes, nucleosomes, histone modifications, DNA methylation, and parts of the three-dimensional architecture of genomes, which could create an enormous combinatorial complexity across the genome. However, many proteins and epigenetic marks are known to colocalize, suggesting that the information content encoded in these marks can be compressed. It has so far proved difficult to understand this compression in a systematic and quantitative manner. Here, we show that simple linear models can reliably predict the data generated by the ENCODE and Roadmap Epigenomics consortia. Further, we demonstrate that a small number of marks can predict all other marks with high average correlation across the genome, systematically revealing the substantial information compression that is present in different cell lines. We find that the linear models for activating marks are typically cell line-independent, while those for silencing marks are predominantly cell line-specific. Of particular note, a nuclear receptor corepressor, transducin beta-like 1 X-linked receptor 1 (TBLR1), was highly predictive of other marks in two hematopoietic cell lines. The methodology presented here shows how the potentially vast complexity of TFs, coregulators, and epigenetic marks at eukaryotic genes is highly redundant and that the information present can be compressed onto a much smaller subset of marks. These findings could be used to efficiently characterize cell lines and tissues based on a small number of diagnostic marks and suggest how the DNA microstates, which regulate the expression of individual genes, can be specified.

| S-EPMC5720766 | biostudies-literature

Transcription factors and molecular epigenetic marks underlying EpCAM overexpression in ovarian cancer.

Project description:BackgroundThe epithelial cell adhesion molecule (EpCAM) is overexpressed on carcinomas, and its downregulation inhibits the oncogenic potential of multiple tumour types. Here, we investigated underlying mechanisms of epcam overexpression in ovarian carcinoma.MethodsExpression of EpCAM and DNA methylation (bisulphite sequencing) was determined for ovarian cancer cell lines. The association of histone modifications and 16 transcription factors with the epcam promoter was analysed by chromatin immunoprecipitation. Treatment with 5-Aza-2'-deoxycytidine (5-AZAC) was used to induce EpCAM expression.ResultsExpression of EpCAM was correlated with DNA methylation and histone modifications. Treatment with 5-AZAC induced EpCAM expression in negative cells. Ten transcription factors were associated with the epcam gene in EpCAM expressing cells, but not in EpCAM-negative cells. Methylation of an Sp1 probe inhibited the binding of nuclear extract proteins in electromobility shift assays; such DNA methylation sensitivity was not observed for an NF-κB probe.ConclusionThis study provides insights in transcriptional regulation of epcam in ovarian cancer. Epigenetic parameters associated with EpCAM overexpression are potentially reversible, allowing novel strategies for sustained silencing of EpCAM expression.

| S-EPMC3142811 | biostudies-literature

Regulatory RNA Apela Is a Component of a Negative Feedback Loop Regulating p53-Mediated Apoptosis in Embryonic Stem Cells (III)

Project description:The goal is to identify RNAs that bind to Hnrnpl (hnRNP L) using RNA immunoprecipitation (RIP) assay.

2015-06-05 | GSE62378 | GEO

Combinatorial role of two paralogous splicing factors, hnRNP L and L-like, in multiple-exon regulation of CD45 alternative splicing

Project description:The goal of this study was to investigate the role of hnRNP L-like in alternative pre-mRNA splicing in human B-cells through an RNA-Seq approach.

2012-03-29 | GSE33013 | GEO

Histone variant macroH2A marks embryonic differentiation in vivo and acts as an epigenetic barrier to induced pluripotency.

Project description:How cell fate becomes restricted during somatic cell differentiation is a long-lasting question in biology. Epigenetic mechanisms not present in pluripotent cells and acquired during embryonic development are expected to stabilize the differentiated state of somatic cells and thereby restrict their ability to convert to another fate. The histone variant macroH2A acts as a component of an epigenetic multilayer that heritably maintains the silent X chromosome and has been shown to restrict tumor development. Here we show that macroH2A marks the differentiated cell state during mouse embryogenesis. MacroH2A.1 was found to be present at low levels upon the establishment of pluripotency in the inner cell mass and epiblast, but it was highly enriched in the trophectoderm and differentiated somatic cells later in mouse development. Chromatin immunoprecipitation revealed that macroH2A.1 is incorporated in the chromatin of regulatory regions of pluripotency genes in somatic cells such as mouse embryonic fibroblasts and adult neural stem cells, but not in embryonic stem cells. Removal of macroH2A.1, macroH2A.2 or both increased the efficiency of induced pluripotency up to 25-fold. The obtained induced pluripotent stem cells reactivated pluripotency genes, silenced retroviral transgenes and contributed to chimeras. In addition, overexpression of macroH2A isoforms prevented efficient reprogramming of epiblast stem cells to naïve pluripotency. In summary, our study identifies for the first time a link between an epigenetic mark and cell fate restriction during somatic cell differentiation, which helps to maintain cell identity and antagonizes induction of a pluripotent stem cell state.

| S-EPMC3585521 | biostudies-literature

Reader interactome of epigenetic histone marks in birds

Project description:Lysine methylation is part of the posttranscriptional histone code employed to recruit modification specific readers to chromatin. Unbiased, quantitative mass spectrometry approaches combined with peptide pull-downs have been used to study histone methylation-dependent binders in mammalian cells. Here, we extend the study to birds by investigating the interaction partners for H3K4me3, H3K9me3, H3K27me3 and H3K36me3 in chicken (gallus gallus) and zebra finch (taeniopygia guttata) using label free quantitative proteomics. In general, we find very strong overlap in interaction partners for the trimethyl marks in birds compared to mammals, underscoring the known conserved function of these modifications. In agreement with their epigenetic role, we find binding of PHF2 and members of the TFIID, SAGA, SET1 and NURF complex to the activation mark H3K4me3. Our data furthermore supports the existence of a LID complex in vertebrates recruited to the H3K4me3. The repressive marks are bound by the HP1 proteins and the EED subunit of the PRC2 complex as well as by WIZ. Like the screens in mammals, we found ZNF462, ZNF828 and POGZ enriched at H3K9me3. However, we noted some unexpected differences. First, we did not observe the enrichment of CDYL and CDYL2 at the repressive marks. Second N-PAC (also known as GLYR1), an H3K36me3 interactor in mammals, is not binding to this modification in our screen. This suggests that despite strong conservation of the histone tail sequence, species-specific differences in epigenetic readers may have evolved.

2016-01-04 | PXD002282 | Pride

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