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Here, we investigate the role of p63 in epithelial differentiation, using an in vitro ES cell model that mimics the early embryonic steps of epidermal development.
The acquisition of a sexual phenotype depends on critical embryonic steps, which initially commit the bipotential gonad to either a testis or an ovary and direct normal morphogenesis of external genitalia.
We evaluated by PCR whether the reprogramming of fibroblasts to blood process was associated with any of these distinct embryonic steps.
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Specifically, accurate studies on heart valve embryonic developmental steps fostered the implementation of the manufacturing process with cues essential for a boosted cell differentiation [ 9– 11].
Satellite cell activation and differentiation during regeneration recapitulate embryonic developmental steps based on similar regulatory mechanisms, but in a completely different environment.
Our studies provide novel mechanistic insights into the pathogenesis of AEC syndrome and establish a functional link between FGF signalling and p63 in the expansion of epithelial progenitor cells during embryonic development, a step required for skin and palate morphogenesis.
Significantly, a recent report suggested that RDH10 might catalyse the first oxidation step of retinol, a critical step for embryonic RA generation (Sandell et al, 2007).
ES cells are thus an effective tool in recapitulating in vitro the main steps of embryonic development.
We have previously established a cellular model that recapitulates in vitro, the main steps of embryonic neuroectodermal fate (Fig. S1).
Moreover, modelling the early steps of embryonic development in vitro may provide the best approach to produce cell types with native properties.
Bone morphogenetic proteins (BMPs) are members of the transforming growth factor-β (TGF-β) superfamily and are involved in the control of multiple key steps of embryonic development and differentiation [6] [8].
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