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Mus musculus

ABSTRACT: DDX5-deficiency affects cell fate decisions by regulating lineage specific genes and polycomb repressive complexes

PROVIDER: PRJNA308723 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3099530.fastq.gz	Fastqsanger.gz
	SRR3099525.fastq.gz	Fastqsanger.gz
	SRR3099526.fastq.gz	Fastqsanger.gz
	SRR3099528.fastq.gz	Fastqsanger.gz
	SRR3099529.fastq.gz	Fastqsanger.gz

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DDX5-deficiency affects cell fate decisions by regulating lineage specific genes and polycomb repressive complexes

Project description:DDX5-deficiency affects cell fate decisions by regulating lineage specific genes and polycomb repressive complexes

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Helin M.musculus Identification of genes repressed by CBX8 and BMI1

Project description:The polycomb group proteins form large repressive complexes. It has recently become evident, via ChIP on chip analysis, that the polycomb complexes, PRC1 and PRC2, target a large number of genes (Boyer et al., 2006; Bracken et al., 2006; Tolhuis et al., 2006), which are involved in cell fate decisions. In order to identify genes which are truly regulated by the polycomb group proteins, CBX8 and BMI1, we expressed these two proteins in mouse embryonic fibroblasts (MEFs) by retroviral infection.

2007-03-05 | E-MEXP-793 | biostudies-arrayexpress

PRC2 specifies ectoderm lineages and maintains pluripotency in primed but not naïve ESCs

Project description:Polycomb repressive complex 2 and the epigenetic mark that it deposits, H3K27me3, are evolutionarily conserved and play critical roles in development and cancer. However, their roles in cell fate decisions in early embryonic development remain poorly understood. Here we report that knockout of polycomb repressive complex 2 genes in human embryonic stem cells causes pluripotency loss and spontaneous differentiation toward a meso-endoderm fate, owing to de-repression of BMP signalling. Moreover, human embryonic stem cells with deletion of EZH1 or EZH2 fail to differentiate into ectoderm lineages. We further show that polycomb repressive complex 2-deficient mouse embryonic stem cells also release Bmp4 but retain their pluripotency. However, when converted into a primed state, they undergo spontaneous differentiation similar to that of hESCs. In contrast, polycomb repressive complex 2 is dispensable for pluripotency when human embryonic stem cells are converted into the naive state. Our studies reveal both lineage- and pluripotent state-specific roles of polycomb repressive complex 2 in cell fate decisions.

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LFQMS of RING2 (RING1B, RNF2) immunoprecipitation from MDA-MB-231 and T47D breast cancer cells

Project description:Polycomb repressive complex PRC1 is essential for gene regulation in numerous cell fate decisions. We show that RING1B (RING2, RNF2) and canonical PRC1 (cPRC1) genes are amplified and overexpressed in breast cancer (BC). Moreover, cPRC1 complexes functionally associate with genes regulated by cell type specific key transcription factors such as estrogen receptor (ER) in ER+ tumor cells and BRD4 in triple negative BC cells. cPRC1 is recruited to active enhancers in a manner independent of PRC2 and RING1B enzymatic activity. RING1B regulates enhancer activity and gene transcription not only by promoting the expression of BC oncogenes but also by regulating chromatin accessibility for oncogenic transcription factors. RING1B recruitment, and thus PRC1 association, to active enhancers occurs in multiple cancers.

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Project description:Pioneer transcription factors (TFs) regulate cell fate by establishing transcriptionally primed and active states. However, cell fate control requires the coordination of both lineage-specific gene activation and repression of alternative lineage programs, a process that is poorly understood. Here, we demonstrate that the pioneer TF Forkhead box A (FOXA), required for endoderm lineage commitment, coordinates with the PR domain zinc finger 1 (PRDM1) TF to recruit Polycomb repressive complexes, which establish bivalent enhancers and repress alternative lineage programs. Similarly, the pioneer TF OCT4 coordinates with PRDM14 to repress cell differentiation programs in pluripotent stem cells, suggesting this is a common feature of pioneer TFs. We propose that pioneer and PRDM TFs coordinate recruitment of Polycomb complexes to safeguard cell fate.

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Pioneer transcription factors coordinate active and repressive gene expression states to regulate cell fate [CUT&Run and ChIP-seq]

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