Prdm14 promotes germline fate and naive pluripotency by repressing FGF signalling and DNA methylation

被引：123

作者：

Grabole, Nils

Tischler, Julia

Hackett, Jamie A.

Kim, Shinseog

Tang, Fuchou

Leitch, Harry G.

Magnusdottir, Erna

Surani, M. Azim ^{[1
]}

机构：

[1] Univ Cambridge, Canc Res UK Gurdon Inst, Dept Physiol Dev & Neurosci, Wellcome Trust, Cambridge CB2 1QN, England

来源：

EMBO REPORTS | 2013年 / 14卷 / 07期

基金：

英国惠康基金;

关键词：

DNA methylation; FGF signalling; pluripotency; Prdm14; primordial germ cells; EMBRYONIC STEM-CELLS; GROUND-STATE; SELF-RENEWAL; LINEAGE; DYNAMICS; DIFFERENTIATION; BLIMP1;

D O I：

10.1038/embor.2013.67

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：629 / 637

页数：9

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