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Updated: Feb 1, 2026

Protocol for Human Blastoids Modeling Blastocyst Development and Implantation
Published on: August 10, 2022
FGFR1 regulates trophectoderm development and facilitates blastocyst implantation
Agata Kurowski1, Andrei Molotkov1, Philippe Soriano1
1Department of Cell, Developmental, and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States.
Fibroblast growth factor receptor (FGFR) signaling is crucial for mammalian development. Loss of FGFR1 or both FGFR1 and FGFR2 in mice causes early embryonic lethality due to impaired trophectoderm differentiation and implantation defects.
Area of Science:
- Developmental Biology
- Genetics
- Cell Biology
Background:
- Fibroblast growth factor (FGF) signaling, mediated by FGF receptors (FGFRs), is essential for mammalian development.
- FGFR1 and FGFR2 play critical roles, with mutations leading to developmental abnormalities and lethality.
Purpose of the Study:
- To investigate the roles of FGFR1 and FGFR2 in trophectoderm (TE) development.
- To understand the basis for peri-implantation lethality in Fgfr1 knockout mouse models.
Main Methods:
- Generation and analysis of Fgfr1 and Fgfr2 knockout mouse embryos.
- In vivo assessment of TE cell behavior, including CDX2 expression and E-Cadherin polarity.
- In vitro derivation and differentiation of mutant trophoblast stem cells (TSCs).
Main Results:
- Fgfr1-/- and Fgfr1-/-Fgfr2-/- embryos exhibit peri-implantation lethality.
- Fgfr1-/- TE cells show defects in CDX2 downregulation and apicobasal polarity.
- Mutant TSCs could not be derived from Fgfr1-/-Fgfr2-/- blastocysts, and Fgfr1-/- TSCs had impaired differentiation.
Conclusions:
- FGFR1 and FGFR2 signaling are critical for proper TE differentiation and function.
- Compromised TE differentiation in Fgfr1 mutants leads to implantation defects and embryonic lethality.
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