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

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

PROVIDER: PRJNA255384 | ENA |

REPOSITORIES: ENA

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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 [Affymetrix Expression]

2015-07-15 | GSE59464 | GEO

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

PRMT5-mediated histone arginine methylation antagonizes transcriptional repression by polycomb complex PRC2

Project description:PRMT5-mediated histone arginine methylation antagonizes transcriptional repression by polycomb complex PRC2

| PRJNA598218 | ENA

PRMT5-mediated histone arginine methylation antagonizes transcriptional repression by polycomb complex PRC2 (RNA-seq)

Project description:PRMT5-mediated histone arginine methylation antagonizes transcriptional repression by polycomb complex PRC2 (RNA-seq)

| PRJNA547829 | ENA

PRMT5-mediated histone arginine methylation antagonizes transcriptional repression by polycomb complex PRC2 (ChIP-seq)

Project description:PRMT5-mediated histone arginine methylation antagonizes transcriptional repression by polycomb complex PRC2 (ChIP-seq)

| PRJNA598220 | ENA

Accurate H3K27 methylation patterns can be established de novo by SUZ12-directed PRC2

Project description:The Polycomb repressive complex 2 (PRC2) catalyzes H3K27 methylation and is required for maintaining transcriptional patterns and cellular identity, but the specification and maintenance of genomic PRC2 binding and H3K27 methylation patterns remain incompletely understood. Epigenetic mechanisms have been proposed, wherein pre-existing H3K27 methylation directs recruitment and regulates the catalytic activity of PRC2 to support its own maintenance. Here we investigate if such mechanisms are required for specifying H3K27 methylation patterns in mouse embryonic stem cells. Through genetic knockouts of subunits, we find that PRC2 is responsible for all levels of H3K27 methylation, and that methylation patterns can be accurately established de novo, when a subunit is reintroduced in the absence of pre-existing H3K27 methylation and PRC2 chromatin binding. Furthermore, we find that the core-subunit SUZ12 directs genomic binding of PRC2, which is essential for establishing correct methylation patterns.

2018-01-12 | GSE103685 | GEO

PRMT5-mediated histone arginine methylation antagonizes transcriptional repression by polycomb complex PRC2.

Project description:Protein arginine methyltransferase 5 (PRMT5) catalyzes the symmetric di-methylation of arginine residues in histones H3 and H4, marks that are generally associated with transcriptional repression. However, we found that PRMT5 inhibition or depletion led to more genes being downregulated than upregulated, indicating that PRMT5 can also act as a transcriptional activator. Indeed, the global level of histone H3K27me3 increases in PRMT5 deficient cells. Although PRMT5 does not directly affect PRC2 enzymatic activity, methylation of histone H3 by PRMT5 abrogates its subsequent methylation by PRC2. Treating AML cells with an EZH2 inhibitor partially restored the expression of approximately 50% of the genes that are initially downregulated by PRMT5 inhibition, suggesting that the increased H3K27me3 could directly or indirectly contribute to the transcription repression of these genes. Indeed, ChIP-sequencing analysis confirmed an increase in the H3K27me3 level at the promoter region of a quarter of these genes in PRMT5-inhibited cells. Interestingly, the anti-proliferative effect of PRMT5 inhibition was also partially rescued by treatment with an EZH2 inhibitor in several leukemia cell lines. Thus, PRMT5-mediated crosstalk between histone marks contributes to its functional effects.

| S-EPMC7102951 | biostudies-literature

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