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First published online October 6, 2003
doi: 10.1242/10.1242/dev.00788
1 Cancer Research UK, London Research Institute, 61 Lincoln's Inn Fields, London
WC2A 3PX, UK
2 Cell Adhesion and Disease Laboratory, St Thomas Hospital, London SE1 7EH,
UK
Author for correspondence (e-mail:
clive.dickson{at}cancer.org.uk)
Accepted 4 August 2003
To understand the role Fgf signalling in skin and hair follicle development, we analysed the phenotype of mice deficient for Fgfr2-IIIb and its main ligand Fgf10. These studies showed that the severe epidermal hypoplasia found in mice null for Fgfr2-IIIb is caused by a lack of the basal cell proliferation that normally results in a stratified epidermis. Although at term the epidermis of Fgfr2-IIIb null mice is only two to three cells thick, it expresses the classical markers of epidermal differentiation and establishes a functional barrier. Mice deficient for Fgf10 display a similar but less severe epidermal hypoplasia. By contrast, Fgfr2-IIIb–/–, but not Fgf10–/–, mice produced significantly fewer hair follicles, and their follicles were developmentally retarded. Following transplantation onto nude mice, grafts of Fgfr2-IIIb–/– skin showed impaired hair formation, with a decrease in hair density and the production of abnormal pelage hairs. Expression of Lef1, Shh and Bmp4 in the developing hair follicles of Fgfr2-IIIb–/– mice was similar to wild type. These results suggest that Fgf signalling positively regulates the number of keratinocytes needed to form a normal stratified epidermis and to initiate hair placode formation. In addition, Fgf signals are required for the growth and patterning of pelage hairs.
Key words: Fgfr2-IIIb, Skin, Epidermis, Hair follicle, Hair differentiation, Mouse
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