| Literature DB >> 30552867 |
Agata Kurowski1, Andrei Molotkov1, Philippe Soriano2.
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.Entities:
Keywords: FGF; TS cells; Trophectoderm
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Year: 2018 PMID： 30552867 PMCID： PMC6370302 DOI： 10.1016/j.ydbio.2018.12.008
Source DB: PubMed Journal: Dev Biol ISSN： 0012-1606 Impact factor: 3.582