A PRC2-Dependent Repressive Role of PRDM14 in Human Embryonic Stem Cells and Induced Pluripotent Stem Cell Reprogramming

重编程 PRC2 生物 诱导多能干细胞 胚胎干细胞 细胞生物学 干细胞 染色质 遗传学 基因 组蛋白H3
作者
Yun-Shen Chan,Jonathan Göke,Xinyi Lu,Nandini Venkatesan,Bo Feng,I-hsin Su,Huck‐Hui Ng
出处
期刊:Stem Cells [Oxford University Press]
卷期号:31 (4): 682-692 被引量:69
标识
DOI:10.1002/stem.1307
摘要

Abstract PRDM14 is an important determinant of the human embryonic stem cell (ESC) identity and works in concert with the core ESC regulators to activate pluripotency-associated genes. PRDM14 has been previously reported to exhibit repressive activity in mouse ESCs and primordial germ cells; and while PRDM14 has been implicated to suppress differentiation genes in human ESCs, the exact mechanism of this repressive activity remains unknown. In this study, we provide evidence that PRDM14 is a direct repressor of developmental genes in human ESCs. PRDM14 binds to silenced genes in human ESCs and its global binding profile is enriched for the repressive trimethylation of histone H3 lysine 27 (H3K27me3) modification. Further investigation reveals that PRDM14 interacts directly with the chromatin regulator polycomb repressive complex 2 (PRC2) and PRC2 binding is detected at PRDM14-bound loci in human ESCs. Depletion of PRDM14 reduces PRC2 binding at these loci and the concomitant reduction of H3K27me3 modification. Using reporter assays, we demonstrate that gene loci bound by PRDM14 exhibit repressive activity that is dependent on both PRDM14 and PRC2. In reprogramming human fibroblasts into induced pluripotent stem cells (iPSCs), ectopically expressed PRDM14 can repress these developmental genes in fibroblasts. In addition, we show that PRDM14 recruits PRC2 to repress a key mesenchymal gene ZEB1, which enhances mesenchymal-to-epithelial transition in the initiation event of iPSC reprogramming. In summary, our study reveals a repressive role of PRDM14 in the maintenance and induction of pluripotency and identifies PRDM14 as a new regulator of PRC2.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
榕俊发布了新的文献求助10
刚刚
科研通AI6.4的应助被ywb采纳,获得10
1秒前
17完成签到 ,获得积分10
2秒前
2秒前
2秒前
CipherSage的应助被YXY采纳,获得10
3秒前
兰惟提发布了新的文献求助10
3秒前
Shine完成签到,获得积分10
4秒前
ny66的应助被genghailun采纳,获得10
4秒前
yyyy完成签到 ,获得积分10
5秒前
5秒前
sft发布了新的文献求助10
6秒前
6秒前
7秒前
9秒前
再找找发布了新的文献求助10
12秒前
12秒前
到处找文献写综述完成签到,获得积分10
13秒前
时光的猫完成签到,获得积分10
13秒前
15秒前
Hello的应助被光工刘采纳,获得30
16秒前
16秒前
尤静柏完成签到,获得积分10
17秒前
17秒前
温婉的亦旋完成签到,获得积分10
18秒前
20秒前
左右是个疯子完成签到,获得积分20
21秒前
v0id的应助被dje采纳,获得10
21秒前
22秒前
22秒前
科研通AI6.2的应助被再找找采纳,获得10
23秒前
田様的应助被xelloss采纳,获得10
24秒前
fffxj完成签到,获得积分10
25秒前
26秒前
Ava的应助被仔仔采纳,获得10
27秒前
eeeeeeee完成签到,获得积分10
27秒前
Yoeyvol发布了新的文献求助30
28秒前
郑板桥完成签到,获得积分10
29秒前
甜甜莆完成签到,获得积分10
29秒前
29秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Aspects of Post-SPE Phonology 2000
Nanocomposite Removal of Pesticides from Wastewater 1000
Rosenblum, Global Change Biology 800
Final Report for the 2-D Test of Model 901 Rotor and Wing Airfoils (BSWT 592) 528
Berberine regulates the TLR4 signaling pathway to suppress hypoxia-induced proliferation and migration of pulmonary arterial smooth muscle cells 520
Organizational Behavior 510
热门求助领域 (近24小时)
化学 材料科学 医学 生物 计算机科学 工程类 纳米技术 物理 有机化学 化学工程 内科学 生物化学 复合材料 催化作用 心理学 细胞生物学 无机化学 电极 光电子学 人工智能
热门帖子
关注 科研通微信公众号,转发送积分 7898433
求助须知:如何正确求助?哪些是违规求助? 9406548
关于积分的说明 20872610
捐赠科研通 7501466
什么是DOI,文献DOI怎么找? 3360022
关于科研通互助平台的介绍 2498143
邀请新用户注册赠送积分活动 2389535