Ras-MAPK signaling promotes trophectoderm formation from embryonic stem cells and mouse embryos

被引：132

作者：

Lu, Chi-Wei ^{[1
,2
,3
]}

Yabuuchi, Akiko ^{[1
,2
,3
]}

Chen, Lingyi ^{[1
,2
,3
]}

Viswanathan, Srinivas ^{[1
,2
,4
]}

Kim, Kitai ^{[1
,2
,3
]}

Daley, George Q. ^{[1
,2
]}

机构：

[1] Childrens Hosp, Div Pediat Hematol & Oncol, Boston, MA 02115 USA

[2] Dana Farber Canc Inst, Boston, MA 02115 USA

[3] Harvard Univ, Stem Cell Inst, Boston, MA 02115 USA

[4] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA

来源：

NATURE GENETICS | 2008年 / 40卷 / 07期

关键词：

D O I：

10.1038/ng.173

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

In blastocyst chimeras, embryonic stem (ES) cells contribute to embryonic tissues but not extraembryonic trophectoderm. Conditional activation of HRas1(Q61L) in ES cells in vitro induces the trophectoderm marker Cdx2 and enables derivation of trophoblast stem (TS) cell lines that, when injected into blastocysts, chimerize placental tissues. Erk2, the downstream effector of Ras-mitogen-activated protein kinase (MAPK) signaling, is asymmetrically expressed in the apical membranes of the 8-cell-stage embryo just before morula compaction. Inhibition of MAPK signaling in cultured mouse embryos compromises Cdx2 expression, delays blastocyst development and reduces trophectoderm outgrowth from embryo explants. These data show that ectopic Ras activation can divert ES cells toward extraembryonic trophoblastic fates and implicate Ras-MAPK signaling in promoting trophectoderm formation from mouse embryos.

引用

页码：921 / 926

页数：6

共 30 条

[1]

Auman HJ, 2002, DEVELOPMENT, V129, P2733

[2] Signaling mechanisms regulating self-renewal and differentiation of pluripotent embryonic stem cells [J].