Fibroblast growth factor 2 can replace ectodermal signaling for feather development.

• DOI: 10.1073/pnas.93.19.10246
• Publication Date: 2002-07-26T14:34:16Z
• Authors: H Song; Y Wang; P F Goetinck
• Keywords: 0301 basic medicine; 0303 health sciences; Transcription, Genetic; Gene Expression Regulation, Developmental; Receptor Protein-Tyrosine Kinases; Chick Embryo; Feathers; Receptors, Fibroblast Growth Factor; 03 medical and health sciences; Ectoderm; Skin Abnormalities; Animals; Fibroblast Growth Factor 2; Receptor, Fibroblast Growth Factor, Type 1; In Situ Hybridization; Signal Transduction; Skin

The initiation and morphogenesis of cutaneous appendages depend on a series of reciprocal signaling events between the epithelium and mesenchyme of the embryonic skin. In the development of feather germs, early dermal signals induce the formation of epidermal placodes that in turn signal the mesoderm to form dermal condensations immediately beneath them. We find a spatially and temporally restricted pattern of transcription for the genes that encode fibroblast growth factor (FGF) 2 and FGF receptor (FGFR) 1 in developing feather germs of the chicken embryo. FGF-2 expression is restricted to the epidermal placodes, whereas FGFR-1 expression is limited to the dermal condensations. Transcription of these genes could not be detected in skins of scaleless (sc/sc) embryos that fail to develop feathers as a result of an ectodermal defect. Treatment of sc/sc skins with FGF-2 results in the formation of feathers at the site of application of the growth factor and the induced feathers express FGFR-1 in their dermal condensations. Thus, we have established FGF-2 as an epidermal signal in early feather germ formation. The observation that FGF-2 can rescue the mutant phenotype of sc/sc embryos suggests that FGF-2 either is, or is downstream from, the signal that the sc/sc mutant ectoderm fails to generate.