Distinct Requirements for FGFR1 and FGFR2 in Primitive Endoderm Development and Exit from Pluripotency

Publication date: Available online 25 May 2017
Source:Developmental Cell
Author(s): Andrei Molotkov, Pierre Mazot, J. Richard Brewer, Ryan M. Cinalli, Philippe Soriano
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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Teaser

FGF4/ERK signaling is known to regulate primitive endoderm development at preimplantation stages. Molotkov et al. show that FGFR1 and FGFR2 are both required for this process, with a predominant role for FGFR1. FGFR1 signaling in ESCs is required for exit from pluripotency and for attaining the primed state.


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