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

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

PROVIDER: PRJNA839383 | ENA |

REPOSITORIES: ENA

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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 [RNA-seq]

Project description: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.

2022-06-10 | GSE203305 | GEO

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

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 ChIPseq - HEK239

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

2018-01-24 | E-MTAB-6006 | biostudies-arrayexpress

PRC1.6 RNAseq

Project description:PRC1.6 RNAseq

| PRJEB65039 | ENA

PRC1.6 ChIPseq - mouse ES

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

2018-01-24 | E-MTAB-6007 | biostudies-arrayexpress

PRC1.6 molecule L3MBTL2 protects MYCN-amplified neuroblastoma cells via epigenetic gene suppression

Project description:Polycomb-group complexes are evolutionarily conserved epigenetic machineries that regulate stem cell fate decisions/development and are also implicated in tumorigenesis mainly by histone modification. PRC1 complexes mediates ubiquitylation of histone H2A on lysine 119 and consists of PRC1.1 to PRC1.6 complexes. Here, we studied the functional roles of a PRC1.6 molecule L3MBTL2 in neuroblastoma (NB) cells. L3MBTL2 knockout- and knockdown-experiments elucidated that L3MBTL2 depletion suppressed NB cell proliferation according with cell cycle arrest and gamma-H2A up-regulation. L3MBTL2 knockout profoundly suppressed xenograft tumor formation. Transcriptome analysis detected the suppressed cell cycle-related pathways and the activated the differentiation-related pathways. The remarkable de-repressed genes by the L3MBTL2 knockout were BRME1 and NRIP3. ChIP experiments showed co-localization of the PRC1.6 components PCGF6/E2F6/L3MBTL2 and MYCN at the transcription start sites (TSS) of these genes. L3MBTL2 knockout reduced H2AK119ub marks at the TSS regions but PCGF6 binding was heterogeneously changed. This study clarified the significance of PRC1.6 molecule L3MBTL2 in NB cell homeostasis and the epigenetic mechanism of the L3MBTL2-mediated gene suppression in NB that regulates the PRC1.6 complex localization and H2AK119 mono-ubiquitination in a gene locus-specific manner.

2023-09-26 | GSE201512 | GEO

Rif1 and Hmgn3 Regulate Conversion of Murine Trophoblast Stem Cells

Project description:The arising of trophectoderm (TE) is a hallmark event in preimplantation development during embryogenesis. However, little is known about the mechanisms underlying TE specification. Our findings demonstrate that depletion of Rif1 breaks down the barriers to conversion of trophoblast stem cells (TSCs). Rif1-null induced TSCs show typical TE properties, and differentiation potentials to terminal trophoblast lineages. Global transcriptome analysis reveals that Rif1-null activates 2-cell embryo (2C) related genes and induces a totipotent-like state, which is probably the main reason for the conversion of TSCs from Rif1-null embryonic stem cells (ESCs). Chimeric assays further confirm that Rif1-null ESCs can contribute to TE, further yielding TSCs in vitro. Over-expression of a downstream gene of Rif1, Hmgn3, can also activate 2C related genes and facilitate induction of TSCs. Here, we report two pioneer genes regulating conversion of TSCs and provide insights for investigating the mechanisms of TE specification.

2021-12-01 | GSE189683 | GEO

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