Distinct Requirements for FGFR1 and FGFR2 in Primitive Endoderm Development and Exit from Pluripotency
Open accessAbstract
Activation of the FGF signaling pathway during preimplantation development of the mouse embryo is known to be essential for differentiation of the inner cell mass and the formation of the primitive endoderm (PrE). We now show using fluorescent reporter knockin lines that Fgfr1 is expressed in all cell populations of the blastocyst, while Fgfr2 expression becomes restricted to extraembryonic lineages, including the PrE. We further show that loss of both receptors prevents the development of the PrE and demonstrate that FGFR1 plays a more prominent role in this process than FGFR2. Finally, we document an essential role for FGFRs in embryonic stem cell (ESC) differentiation, with FGFR1 again having a greater influence than FGFR2 in ESC exit from the pluripotent state. Collectively, these results identify mechanisms through which FGF signaling regulates inner cell mass lineage restriction and cell commitment during preimplantation development.
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FGF4 signaling is active across the ICM population and is critical for PrE specification.
“While active across the ICM population25–27, FGF4 signaling is critical for PrE specification28,29.”
From The emergent landscape of the mouse gut endoderm at single-cell resolution (2019) · cites this paper as [26]
The citation is attached to the claim that FGF4 signaling is critical for PrE specification, not to the preceding claim about activity across the ICM. The Discussion says FGF4 promotes conversion of ICM cells toward a PrE fate. However, the Results section “Fgfr1 and Fgfr2 are Required for Maintenance but not Initiation of the PrE” says PrE development begins without FGF signaling but is not maintained, so the claim overstates its role in initial specification. Page numbers were not available in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredMouse mutants in Fgfr1 and Fgfr2 phenocopy embryos lacking Fgf4, with defects in PrE specification and exit from naïve pluripotency in EPI.
“Mouse mutants in both Fgfr1 and Fgfr2 phenocopy embryos lacking Fgf4, with defects in PrE specification and exit from naïve pluripotency in the EPI26,27,29.”
From The emergent landscape of the mouse gut endoderm at single-cell resolution (2019) · cites this paper as [26]
The Results (page unavailable) say Fgfr1/Fgfr2 double-null embryos phenocopy Fgf4-null embryos in disrupted PrE development. The Discussion (page unavailable) says PrE cells appear to be specified but not maintained, contrary to the claim of defective specification. It also reports persistent Nanog in mutant embryos and proposes impaired EPI maturation, while the direct exit-from-pluripotency experiments used ES cells. (LLM, conf=0.88)
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- Authors
- Molotkov, A., Mazot, P., Brewer, J. R., Cinalli, R. M., & Soriano, P.
- Affiliations
- Tisch Cancer Institute (US)
- Corresponding author
- Soriano, Philippe
- ORCID
- Soriano, Philippe
- Venue
- Developmental Cell
- Publisher
- Elsevier BV
- Published
- 2017-06
- Volume
- 41
- Issue
- 5
- Pages
- 511-526.e4
- ISSN
- 1534-5807 (ISSN-L)
- PMC
- PMC5502766
- OpenAlex
- W2618900678
- Cited by
- 177
- References
- 70
- Citations by year
- 2026: 12 · 2025: 18 · 2024: 15 · 2023: 19 · 2022: 19 · 2021: 21 · 2020: 24 · 2019: 18 · 2018: 24 · 2017: 7
- FWCI
- 7.95
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Developmental Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Tisch Cancer Institute (P30 CA196521)
- NIH (RO1 DE022778)
- NYSTEM (IIRP N11G-131)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fibroblast Growth Factor Research
- Keywords
- FGFR1, FGFR2, FGF signaling, primitive endoderm, exit from pluripotency, embryonic stem cell differentiation, preimplantation embryo development, blastocyst, inner cell mass, extraembryonic lineages, lineage restriction, lineage commitment
- MeSH terms
- Animals, Cell Differentiation, Cells, Cultured, Embryo, Mammalian, Endoderm, Female, Humans, Mice, Inbred C57BL, Signal Transduction, Mice, Knockout, Cell Lineage, Mice, Receptor, Fibroblast Growth Factor, Type 1, Receptor, Fibroblast Growth Factor, Type 2, Fibroblast Growth Factor 4, Embryonic Stem Cells, Blastocyst Inner Cell Mass
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