(Secondary Ownership. The experiment uses only third-party data.)
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
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