期刊
DEVELOPMENTAL BIOLOGY
卷 446, 期 1, 页码 94-101出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2018.12.008
关键词
FGF; Trophectoderm; TS cells
资金
- Tisch Cancer Institute at Mount Sinai (Cancer Center Support Grant) [P30 CA196521]
- NYSTEM [IIRP N11G-131]
- NIH/NCI [RO1 DE022778]
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.
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