FGF/ERK signaling pathway: how it operates in mammalian preimplantation embryos and embryo-derived stem cells.

The integration of extracellular signals and lineage-specific transcription factors allows cells to react flexibly to their environment, thus endowing the mammalian embryo with the capacity of regulative development. The combination of genetic and pharmacological tools allowing disruption of the fibroblast growth factor / extracellular signal-regulated kinase (FGF/ERK) pathway, together with animal models expressing lineage-specific reporters provided new insights into the role of this signaling cascade during mammalian development, as well as in embryo-derived stem cells. Here, we combine current knowledge acquired from different mammalian models to consider the universality of this cascade in specifying cellular fate across mammalian species.

The Regulative Nature of Mammalian Embryos.

The striking developmental plasticity of early mammalian embryos has been known since the classical experiments performed in the 1950s and 1960s. There are many lines of evidence that the mammalian embryo is able to continue normal development even when exposed to severe experimental manipulations of the number and position of cells within the embryo. These observations have raised the question about the mechanisms involved in emergence, maintenance, and progressive restriction of this plasticity. Only recently, we have begun to understand these mechanisms. In this review, in order to explain the molecular and cellular events underlying the remarkable plasticity of the early mammalian embryo, we discuss results of classical experiments demonstrating developmental potential of mammalian embryos and link them with the novel data provided by contemporary experimental approaches. We also show how developmental flexibility of mammalian embryos is manifested in nature, and discuss its implications for basic research and medicine.