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Prdm14 promotes germline fate and naive pluripotency by repressing FGF signalling and DNA methylation
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Prdm14 promotes germline fate and naive pluripotency by repressing FGF signalling and DNA methylation
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Journal Article
Prdm14 promotes germline fate and naive pluripotency by repressing FGF signalling and DNA methylation
2013
Overview
Primordial germ cells (PGCs) and somatic cells originate from postimplantation epiblast cells in mice. As pluripotency is lost upon differentiation of somatic lineages, a naive epigenome and the pluripotency network are re‐established during PGC development. Here we demonstrate that
Prdm14
contributes not only to PGC specification, but also to naive pluripotency in embryonic stem (ES) cells by repressing the DNA methylation machinery and fibroblast growth factor (FGF) signalling. This indicates a critical role for
Prdm14
in programming PGCs and promoting pluripotency in ES cells.
The transcription factor
Prdm14
is a critical regulator of pluripotency and germline development. This study shows that
Prdm14
represses DNA methylation and FGF signaling, thereby promoting both germ cell fate and naive pluripotency in ESC.
Publisher
John Wiley & Sons, Ltd,Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group
Subject
/ Bacteria
/ DNA
/ EMBO09
/ EMBO11
/ Embryonic Stem Cells - cytology
/ Embryonic Stem Cells - metabolism
/ Fibroblast Growth Factors - genetics
/ Fibroblast Growth Factors - metabolism
/ Gene Expression Regulation, Developmental
/ Genomics
/ Mice
/ Mitogen-Activated Protein Kinases - genetics
/ Mitogen-Activated Protein Kinases - metabolism
/ Pluripotent Stem Cells - cytology
/ Pluripotent Stem Cells - metabolism
/ Prdm14
