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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data of embryonic stem (ES) cells from both control and Prmt6 overexpressed population

ABSTRACT: ES cells are able to self-renew and remain pluripotent. These characteristics are maintained by both genetic and epigenetic regulators. Protein arginine methyltransferase (PRMT) 4 and 5 are shown to be important in early embryonic development and in ES cells. PRMT6-mediated di-methylation of histone H3 at arginine 2 (H3R2me2) can antagonize the tri-methylation of histone H3 at lysine 4, which marks active genes. However, it is unclear whether PRMT6 and PRMT6-mediated H3R2me2 play crucial roles in early embryonic development and ES cell identity. In this study, we investigate their functions using mouse ES cells as the model. We used microarray (Affymetrix GeneChip Mouse Gene 1.0ST) to examine the global change of gene expression in mouse ES cells when Prmt6 was overexpressed and identified distinct classes of genes that are up-regulated and down-regulated during this process. Mouse ES cells were transfected with either pCAGIP.puro empty vector (control) or Prmt6 overexpressing plasmid (P+6 OE). After 3 days of selection by puromycin, cells from both populations were subjected to RNA extraction and hybridization on Affymetrix microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: Qiang Wu

PROVIDER: E-GEOD-27685 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data of embryonic stem (ES) cells from both control and Prmt6 overexpressed population

Project description:ES cells are able to self-renew and remain pluripotent. These characteristics are maintained by both genetic and epigenetic regulators. Protein arginine methyltransferase (PRMT) 4 and 5 are shown to be important in early embryonic development and in ES cells. PRMT6-mediated di-methylation of histone H3 at arginine 2 (H3R2me2) can antagonize the tri-methylation of histone H3 at lysine 4, which marks active genes. However, it is unclear whether PRMT6 and PRMT6-mediated H3R2me2 play crucial roles in early embryonic development and ES cell identity. In this study, we investigate their functions using mouse ES cells as the model. We used microarray (Affymetrix GeneChip Mouse Gene 1.0ST) to examine the global change of gene expression in mouse ES cells when Prmt6 was overexpressed and identified distinct classes of genes that are up-regulated and down-regulated during this process.

2011-03-04 | GSE27685 | GEO

esBAF is an essential component of the core pluripotency transcriptional network

Project description:Distinctive SWI/SNF-like ATP-dependent chromatin remodeling esBAF complexes are indispensable for the maintenance and pluripotency of mouse embryonic stem (ES) cells. To understand the mechanism underlying the roles of these complexes in ES cells, we performed high-resolution genome-wide mapping of the core ATPase subunit, Brg, using ChIP-Seq technology. We find that that esBAF, as represented by Brg, binds to genes encoding components of the core ES transcriptional circuitry, including Polycomb group proteins. esBAF colocalizes extensively with Oct4, Sox2 and Nanog genome-wide, and shows distinct functional interactions with Oct4 and Sox2 at its target genes. Surprisingly, no significant colocalization of esBAF with PRC2 complexes, represented by Suz12, is observed. Lastly, esBAF co-binds with Stat3 and Smad1 genome-wide, consistent with a direct and critical role in LIF and BMP signaling essential to maintain pluripotency. Taken together, our studies indicate that esBAF is both an essential component of the core pluripotency transcriptional network, and might also be a critical component of the LIF and BMP signaling pathways essential for maintenance of self-renewal and pluripotency. Brg knockdown effect on expression, Brg ChIP-Seq

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Expression data from ES cells

Project description:H2A.B is a unique histone H2A variant that shares only 40 ~ 50 % sequence identity with canonical H2A. It has only been identified in mammals and has quickly evolved with remarkable sequence diversity among different species. H2A.B is ubiquitously expressed in most cells and tissues. It is mainly deposited in gene body region.The localization of H2A.B is associated with methylated CpG islands in mouse ES cells.H2A.B facilitates transcription elongation to go through methylated CpG islands in the gene bodies. One typical example is that H2A.B regulates transcription elongation at imprinted loci. We used microarray to test the function of H2A.B on gene expression. Mouse ES cells infected with control knockdown(KD) or H2A.B KD virus were treated with G418. ES cells were extracted for RNA and hybridization on Affymetrix microarrays.

2013-12-24 | E-GEOD-48446 | biostudies-arrayexpress

Repressive mark H3K27me3 in PRMT6 KO NT2/D1 cells

Project description:Protein arginine methyltransferase 6 (PRMT6) is an epigenetic regulator of fundamental cellular processes, such as gene expression and DNA repair. Asymmetric dimethylation of histone H3 at arginine 2 (H3R2me2a) is the major histone modification catalyzed by PRMT6. To identify the genome-wide deposition and transcriptional impact of H3R2me2a, we established PRMT6 deletion in a human cell model of neural differentiation. These knockout cells show severe neural differentiation defects. ChIP-seq profiling reveals that H3R2me2a is present at promoter as well as non-promoter sites in a PRMT6-dependent manner. Loss of H3R2me2a causes enhanced H3K4me3 deposition and target gene transcription supporting a genome-wide repressive nature of H3R2me2a. Intriguingly, the non-promoter H3R2me2a peaks co-localize with active enhancer marks, such as H3K4me1 and H3K27ac.

2018-09-27 | GSE117341 | GEO

Genomic location of PRMT6-dependent H3R2 methylation is decisive for the transcriptional outcome of associated genes [ChIP-seq]

2018-09-27 | GSE117200 | GEO

Genomic occurrence analysis of PRMT6-dependent H3R2me2a

2018-09-27 | GSE107609 | GEO

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

Genome-wide mapping of Eset-binding sites and H3K9me3 state in mouse embryonic stem cells

Project description:The histone H3 lysine 9 (H3K9) methyltransferase Eset is an epigenetic regulator critical for the development of the inner cell mass (ICM). Although ICM-derived embryonic stem (ES) cells are normally unable to contribute to the trophectoderm (TE) in blastocysts, we find that depletion of Eset by shRNAs leads to differentiation with the formation of trophoblast-like cells and induction of trophoblast-associated gene expression. Using ChIP-seq analyses, we identified Eset target genes with Eset-dependent H3K9 trimethylation. We confirmed that genes that are preferentially expressed in the TE (Tcfap2a and Cdx2) are bound and repressed by Eset. Single cell PCR analysis shows that the expression of Cdx2 and Tcfap2a is also induced in Eset-depleted morula cells. Importantly, Eset-depleted cells can incorporate into the TE of a blastocyst and subsequently placental tissues. Co-immunoprecipitation and ChIP assays further demonstrates that Eset interacts with Oct4, which in turn recruits Eset to silence these trophoblast-associated genes. Our result suggests that Eset restricts the extraembryonic trophoblast lineage potential of pluripotent cells and links an epigenetic regulator to key cell fate decision through a pluripotency factor. Keywords: Epigenetics Examine Eset-binding sites and compare the H3K9me3 state between Eset knockdown mouse ES cells and control knockdown mouse ES cells.

2009-11-04 | E-GEOD-17642 | biostudies-arrayexpress

Dual functions of Tet1 in transcriptional regulation in mouse embryonic stem cells (ChIP-Seq)

Project description:Epigenetic modification of the mammalian genome by DNA methylation (5-methylcytosine) has a profound impact on chromatin structure, gene expression and maintenance of cellular identity. Recent demonstration that members of the Ten-eleven translocation (Tet) family proteins can convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) raised the possibility that Tet proteins are capable of establishing a distinct epigenetic state. We have recently demonstrated that Tet1 is specifically expressed in murine embryonic stem (ES) cells and is required for ES cell self-renewal and maintenance. Using chromatin immunoprecipitation coupled with high-throughput DNA sequencing (ChIP-seq), here we show that Tet1 is preferentially bound to CpG-rich sequences at promoters of both transcriptionally active and Polycomb-repressed genes. Despite a general increase in levels of DNA methylation at Tet1 binding-sites, Tet1 depletion does not lead to down-regulation of all the Tet1 targets. Interestingly, while Tet1-mediated promoter hypomethylation is required for maintaining the expression of a group of transcriptionally active genes, it is also required for repression of Polycomb-targeted developmental regulators. Tet1 contributes to silencing of this group of genes by facilitating recruitment of PRC2 to CpG-rich gene promoters. Thus, our study not only establishes a role for Tet1 in modulating DNA methylation levels at CpG-rich promoters, but also reveals a dual function of Tet1 in promoting transcription of pluripotency factors as well as participating in the repression of Polycomb-targeted developmental regulators. To determine the genome-wide distribution of Tet1 in mouse ES cells, we have performed ChIP-seq experiments using Tet1 antibodies in control knockdown (KD) and Tet1 KD ES cells.

2011-03-30 | E-GEOD-26832 | biostudies-arrayexpress

A mycobacterial effector promotes ferroptosis-dependent pathogenicity and dissemination

Project description:Ferroptosis is an iron-dependent programmed cell death caused by lipid peroxidation. Emerging evidence suggests several pathogens manipulate ferroptosis as a way for pathogen propagation, but the underlying mechanisms remain largely elusive. Here, we report that PtpA, secreted by intracellular pathogen Mycobacterium tuberculosis (Mtb), is a ferroptosis inducer during infection. Mechanistically, Mtb PtpA entries into the nucleus through the RaDAR pathway depending on the conserved cysteine 11 site, but not canonical ARs motif. Then, PtpA functions as an adaptor to increase the affinity between protein arginine methyltransferase 6 (PRMT6) with its substrate histone H3, thus promoting the asymmetric dimethylation of histone H3 at arginine 2 (H3R2me2a), leading to repression of GPX4 gene expression and the ensuing ferroptosis. Accordingly, disrupting nucleus entry site or PRMT6-interacting motif of PtpA markedly eliminates the PtpA-induced ferroptosis in host cells. These findings find a new motif involved in intracellular pathogens effectors for entering host nucleus, and reveal an unrecognized regulatory role of PtpA as an activator of methyltransferases PRMT6 to promote ferroptosis in host nuclear, providing fresh insights into the mechanism of Mtb-induced cell death.

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