| First Author | Kurowski A | Year | 2019 |
| Journal | Dev Biol | Volume | 446 |
| Issue | 1 | Pages | 94-101 |
| PubMed ID | 30552867 | Mgi Jnum | J:270143 |
| Mgi Id | MGI:6276542 | Doi | 10.1016/j.ydbio.2018.12.008 |
| Citation | Kurowski A, et al. (2019) FGFR1 regulates trophectoderm development and facilitates blastocyst implantation. Dev Biol 446(1):94-101 |
| abstractText | 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. |
