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PRC1.6 RNAseq

ABSTRACT: PRC1.6 RNAseq

PROVIDER: PRJEB65039 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2103724.fastq.gz	Fastqsanger.gz
	ERR2103725.fastq.gz	Fastqsanger.gz
	ERR2103726.fastq.gz	Fastqsanger.gz
	ERR2103727.fastq.gz	Fastqsanger.gz
	ERR2103728.fastq.gz	Fastqsanger.gz

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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

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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.

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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.

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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

PRC1.6 RNAseq

Project description:MGA was depleted via Crisper/Cas9 in HEK293 cells and the resulting gene expression changes were profiled.

2018-01-24 | E-MTAB-6005 | biostudies-arrayexpress

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Project description:Conventional crosslinked ChIP was performed on cell lines derived from control (Empty) and sgMga transduced tumors. We wanted to assess PRC1.6 member and MYC binding in the presence and absence of MGA.

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

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