Yamaji2013 Data: PRDM14 Ensures Naive Pluripotency through Dual Regulation of Signaling and Epigenetic Pathways in Mouse Embryonic Stem Cells

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Description from GEO:

Summary Mouse embryonic stem cells (mESCs) fluctuate between a naive inner cell mass (ICM)-like state and a primed epiblast-like state of pluripotency in serum, but are harnessed exclusively in a distinctive, naive state of pluripotency that more faithfully captures the ICM state (the ground state) with inhibitors for mitogen-activated protein kinase (MAPK) and glycogen synthase kinase 3 pathways (2i). Understanding the mechanism ensuring the naive states of pluripotency will be critical to realizing the full potential of ESCs. We show here that PRDM14, a PR domain-containing transcriptional regulator, ensures naive pluripotency by a dual mechanism: Antagonizing fibroblast growth factor receptor (FGFR) signaling that is activated paradoxically by the core transcriptional circuitry for pluripotency and directs a primed state, and repressing de novo DNA methyltransferases that create a primed epiblast-like epigenome. PRDM14 exerts these functions by recruiting polycomb repressive complex 2 (PRC2) specifically to key targets and repressing their expression.

Overall design ChIP-seq of PRDM14 and that of H3K27me3 and SUZ12 on Prdm14 wildtype and knockout ES cells
histone modifications stem cells PRDM ChIP-seq chromatin remodeling transcription factors
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Input Data

Sample Groups and Experimental Factors

Genome Snapshots

'Genome snapshots' are assorted genomic regions that the creators of this experiment considered of particular interest.

Gata4 Locus

Fgfr1 Locus

Dnmt3l Locus

Sox2 Locus

Main Experimental Results

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