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Polycomb PRC2 antagonizes de novo DNA methylation at the maternal Gtl2-Rian-Mirg locus [Affymetrix Expression]

ABSTRACT: Wild-type mouse embryonic stem cells are compared with mutants for components of PRC2 including Ezh2-/-, Eed-/-, and Jarid2-/- cells. Gene expression microarrays were used to compare the expression for these.

ORGANISM(S): Mus musculus

PROVIDER: GSE59464 | GEO | 2015/07/15

SECONDARY ACCESSION(S): PRJNA255386

REPOSITORIES: GEO

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Polycomb PRC2 antagonizes de novo DNA methylation at the maternal Gtl2-Rian-Mirg locus [Affymetrix Expression]

Project description:Wild-type mouse embryonic stem cells are compared with mutants for components of PRC2 including Ezh2-/-, Eed-/-, and Jarid2-/- cells. Gene expression microarrays were used to compare the expression for these. This experiment compares wild-type gene expression with mutants for different PRC2 components, including Ezh2-/-, Eee-/- and Jarid2-/- with two replicates for each using Affymetrix Gene Expression Arrays.

2015-07-15 | E-GEOD-59464 | biostudies-arrayexpress

Polycomb PRC2 antagonizes de novo DNA methylation at the maternal Gtl2-Rian-Mirg locus [Next-Gen Sequence Data]

Project description:Wild-type mouse embryonic stem cells are compared with mutants for components of PRC2 including Ezh2-/-, Eed-/-, and Jarid2-/- cells. Chromatin modifications, Gene expression, Pol-II, small-RNA sequencing, and DNA methylation are compared for both cell types. To study genomic and epigentic control of PRC2 in mESCs, we designed gene expression analysis (RNA-Seq and small RNA-Seq), combining with ChIP-Seq analysis of several factors and histone marks from wild-type and distinct PRC2 mutants including wild-type, Ezh2-/-, Eed-/-, and Jarid2-/-.

2015-07-15 | E-GEOD-59463 | biostudies-arrayexpress

Polycomb PRC2 antagonizes de novo DNA methylation at the maternal Gtl2-Rian-Mirg locus [Next-Gen Sequence Data]

2015-07-15 | GSE59463 | GEO

Polycomb PRC2 antagonizes de novo DNA methylation at the maternal Gtl2-Rian-Mirg locus

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-07-15 | GSE58414 | GEO

PRC2 Is Required to Maintain Expression of the Maternal Gtl2-Rian-Mirg Locus by Preventing De Novo DNA Methylation in Mouse Embryonic Stem Cells.

Project description: Not available

| S-EPMC5384103 | biostudies-literature

Polycomb PRC2 antagonizes de novo DNA methylation at the maternal Gtl2-Rian-Mirg locus

Project description:Polycomb PRC2 antagonizes de novo DNA methylation at the maternal Gtl2-Rian-Mirg locus

| PRJNA255384 | ENA

Hypermethylation and reduced expression of Gtl2, Rian and Mirg at the Dlk1-Dio3 imprinted locus as a marker for poor developmental potential of mouse embryonic stem cells.

Project description: Not available

| S-EPMC7567021 | biostudies-literature

Overexpression of microRNAs from the Gtl2-Rian locus contributes to postnatal death in mice.

Project description: Not available

| S-EPMC5886287 | biostudies-literature

Jarid2 and PRC2, Partner in Regulating Gene Expression

Project description:The Polycomb Group proteins foster gene repression profiles required for proper development and unimpaired adulthood, and comprise the components of the PRC2 complex including the histone H3 lysine 27 (H3K27) methyltransferase Ezh2. How mammalian PRC2 accesses chromatin is unclear. We find that Jarid2 associates with PRC2 and stimulates its enzymatic activity in vitro. Jarid2 contains a Jumonji C domain, but is devoid of detectable histone demethylase activity. Instead, its artificial recruitment to a promoter in vivo resulted in co-recruitment of PRC2 with resultant increased levels of H3K27me2/3. Jarid2 co-localizes with Ezh2 and MTF2, a homologue of Drosophila Pcl, at endogenous genes in ES cells. Jarid2 can itself bind DNA and its recruitment in ES cells is interdependent with that of PRC2 as Jarid2 knockdown reduced PRC2 at its target promoters, and ES cells devoid of the PRC2 component EED are deficient in Jarid2 promoter access. In addition to the well-documented defects in embryonic viability upon down-regulation of Jarid2, ES cell differentiation is impaired, as is Oct4 silencing. Examination of two factors in ES cells

2010-01-01 | E-GEOD-19708 | biostudies-arrayexpress

Two distinct functional axes of positive feedback-enforced PRC2 recruitment in mouse embryonic stem cells

Project description:Polycomb Repressive Complex 2 (PRC2) plays an essential role in development by catalysing trimethylation of histone H3 lysine 27 (H3K27me3), resulting in gene repression. PRC2 consists of two sub-complexes, PRC2.1 and PRC2.2, in which the PRC2 core associates with distinct ancillary subunits such as MTF2 and JARID2, respectively. Both MTF2, present in PRC2.1, and JARID2, present in PRC2.2, play a role in core PRC2 recruitment to target genes in mouse embryonic stem cells (mESCs). However, it remains unclear how these distinct sub-complexes cooperate to establish H3K27me3 domains. Here, we combine a range of Polycomb mutant mESCs with chemical inhibition of PRC2 catalytic activity, to systematically dissect their relative contributions to PRC2 binding to target loci. We find that PRC2.1 and PRC2.2 mediate two distinct paths for recruitment, with mutually reinforced binding. Part of the cross-talk between PRC2.1 and PRC2.2 occurs via their catalytic product H3K27me3, which is bound by the PRC2 core-subunit EED, thereby mediating a positive feedback. Strikingly, removal of either JARID2 or H3K27me3 only has a minor effect on PRC2 recruitment, whereas their combined ablation largely attenuates PRC2 recruitment. This strongly suggests an unexpected redundancy between JARID2 and EED-H3K27me3-mediated recruitment of PRC2. Furthermore, we demonstrate that all core PRC2 recruitment occurs through the combined action of MTF2-mediated recruitment of PRC2.1 to DNA and PRC1-mediated recruitment of JARID2-containing PRC2.2. Both axes of binding are supported by EED-H3K27me3 positive feedback, but to a different degree. Finally, we provide evidence that PRC1 and PRC2 mutually reinforce reciprocal binding. Together, these data disentangle the interdependent and cooperative interactions between Polycomb complexes that are important to establish Polycomb repression at target sites.

2020-08-07 | PXD014290 | Pride

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