FGFR1 regulates trophectoderm development and facilitates blastocyst implantation

Agata Kurowski, Andrei Molotkov, Philippe Soriano

Research output: Contribution to journalArticlepeer-review

24 Scopus citations

Abstract

FGF signaling plays important roles in many aspects of mammalian development. Fgfr1 -/- and Fgfr1 -/- Fgfr2 -/- mouse embryos on a 129S4 co-isogenic background fail to survive past the peri-implantation stage, whereas Fgfr2 -/- embryos die at midgestation and show defects in limb and placental development. To investigate the basis for the Fgfr1 -/- and Fgfr1 -/- Fgfr2 -/- peri-implantation lethality, we examined the role of FGFR1 and FGFR2 in trophectoderm (TE) development. In vivo, Fgfr1 -/- TE cells failed to downregulate CDX2 in the mural compartment and exhibited abnormal apicobasal E-Cadherin polarity. In vitro, we were able to derive mutant trophoblast stem cells (TSCs) from Fgfr1 -/- or Fgfr2 -/- single mutant, but not from Fgfr1 -/- Fgfr2 -/- double mutant blastocysts. Fgfr1 -/- TSCs however failed to efficiently upregulate TE differentiation markers upon differentiation. These results suggest that while the TE is specified in Fgfr1 -/- mutants, its differentiation abilities are compromised leading to defects at implantation.

Original languageEnglish
Pages (from-to)94-101
Number of pages8
JournalDevelopmental Biology
Volume446
Issue number1
DOIs
StatePublished - 1 Feb 2019

Keywords

  • FGF
  • TS cells
  • Trophectoderm

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