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

Chi Wei Lu, Akiko Yabuuchi, Lingyi Chen, Srinivas Viswanathan, Kitai Kim, George Q. Daley

Research output: Contribution to journalArticle

108 Scopus citations

Abstract

In blastocyst chimeras, embryonic stem (ES) cells contribute to embryonic tissues but not extraembryonic trophectoderm. Conditional activation of HRas1Q61L 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.

Original languageEnglish (US)
Pages (from-to)921-926
Number of pages6
JournalNature genetics
Volume40
Issue number7
DOIs
StatePublished - Jul 1 2008
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Genetics

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