Early mammal embryogenesis starts with oocyte fertilization, giving rise to the zygote. The events that the newly formed zygote surpasses are crucial to the embryo developmental success. Shortly after activation of its genome, cells of the embryo segregate into the inner cell mass (ICM) or the trophectoderm (TE). The first will give rise to the embryo while the latter will become the placenta. This first segregation involves cellular and molecular processes that include cell polarity linked to intracellular pathway activation, which will regulate the transcription of trophectoderm-related genes. Then, cells of the ICM undergo the second event of mammalian cell differentiation, which consists of the separation between epiblast (EPI) and hypoblast or primitive endoderm (PrE). This second segregation involves paracrine signaling, leading to differential expression of key genes that will dictate the fate of the cell. Although these processes are described in detail in the mouse, recent studies suggest that the bovine embryo could also be an interesting model for early development, since there are differences to the mouse and similarities with early human embryogenesis. In this review, we gathered the main data available in the literature upon bovine and mouse early development events, suggesting that both models should be analyzed and studied in a complementary way, to better model early events occurring in human development.

The first cellular differentiation event in the pre‐implantation embryo results in the trophectoderm (TE) and the inner cell mass (ICM). A second event occurs in the latter, resulting in the epiblast and the primitive endoderm (PE). This second differentiation is still not fully characterized in bovine development, although it is likely to involve FGF signalling. Thus, in this study, we tested the hypothesis that stimulation or inhibition of the FGF pathway during bovine embryo in vitro culture would only interfere with PE differentiation if maintained until later blastocyst stages. At first, we characterized the expression of PE marker SOX17 at different blastocyst stages. Then, we treated in vitro produced embryos during different windows of time: days 5.0–7.0 (D5–D7), D7–D9, and D5–D9 with 1 μg/ml FGF4 and 1 μg/ml heparin or 1 mM FGFR inhibitor, AZD4547. We observed that the SOX17‐positive cell number only increases in late‐stage blastocysts compared to early stages. Treatment of embryos with FGF4 did not change the number of SOX17‐positive cells, while inhibition of FGFR signalling reduced SOX17‐positive cells from D5–D7 and completely ablated SOX17 expression when kept until D9. In conclusion, FGFR inhibition repressed PE differentiation in bovine embryos at all time points, although stimulation with FGF4 did not interfere with PE cell numbers.