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Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential [RNA-seq]

ABSTRACT: To investigate the cooperative function Rif1 and PRC1.6 complex in the regulation of embryonic development and cell differentiation, we selected embryonic stem cells in which each target gene has been knocked down by shRNA or knocked out conditionally. We then performed gene expression profiling analysis using data obtained from RNA-seq of different samples.

ORGANISM(S): Mus musculus

PROVIDER: GSE203305 | GEO | 2022/06/10

REPOSITORIES: GEO

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Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential [ChIP-seq]

Project description:To investigate if Rif1 depletion compromised the accurate genomic targeting of the PRC1.6 complex, we performed ChIP-seq analyses of Rif1, Pcgf6, RNF2, and the H2AK119ub in the control and Rif1-depleted mESCs.

2022-06-10 | GSE203304 | GEO

Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential

Project description:Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential

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Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential [ChIP-seq]

Project description:Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential [ChIP-seq]

| PRJNA839392 | ENA

Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential [RNA-seq]

Project description:Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential [RNA-seq]

| PRJNA839391 | ENA

PRC1.6 RNAseq

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Project description:Components of the PRC1.6 complex were depleted via Crisper/Cas9 and ChIPed in HEK293 cells.

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Rif1 functions in complex with PRC1.6 to regulate mouse embryonic stem cells fate potential

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

2022-06-09 | GSE203306 | GEO

PRC1.6 and SETDB1-mediated repression of germline genes in the early embryo precedes DNA methylation-mediated silencing.

Project description:Silencing of a subset of germline genes is dependent upon DNA methylation (DNAme) post-implantation. However, these genes are generally hypomethylated in the ICM, implicating alternative silencing pathways before implantation. Indeed, in embryonic stem cells (ESCs), an overlapping set of genes, including germline “genome-defence” (GGD) genes, are upregulated following deletion of the H3K9 methyltransferase SETDB1 or subunits of the non-canonical PRC1 complex PRC1.6. Here, we show that in pre-implantation embryos and naïve ESCs (nESCs), hypomethylated promoters of germline genes bound by the PRC1.6 DNA-binding subunits MGA/MAX/E2F6 are enriched for RING1B-dependent H2AK119ub1 and H3K9me3. Accordingly, silencing of these genes in nESCs shows a greater dependence on PRC1.6 than DNAme. In contrast, GGD genes are hypermethylated in epiblast-like cells and their silencing is dependent upon SETDB1, PRC1.6/RING1B and DNAme, with H3K9me3 and DNAme establishment dependent upon MGA binding. Thus, GGD genes are initially repressed by PRC1.6, with DNAme subsequently engaged in post-implantation embryos.

2021-11-05 | GSE171695 | GEO

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