A crucial role for Fgfr2-IIIb signalling in epidermal development and hair follicle patterning
| Autor: | Kairbaan Hodivala-Dilke, Anita Petiot, Clive Dickson, Francesco J. A. Conti, Jean-Michel Revest, Richard Grose |
|---|---|
| Přispěvatelé: | Aquitaine |
| Jazyk: | angličtina |
| Rok vydání: | 2003 |
| Předmět: |
MESH: Signal Transduction
medicine.medical_specialty MESH: Receptor Fibroblast Growth Factor Type 2 [SDV]Life Sciences [q-bio] Biology MESH: Receptors Fibroblast Growth Factor Fibroblast growth factor Mice 03 medical and health sciences Internal medicine medicine Animals MESH: Animals Receptor Fibroblast Growth Factor Type 2 Molecular Biology MESH: Mice 030304 developmental biology 0303 health sciences FGF10 Epidermis (botany) integumentary system 030302 biochemistry & molecular biology Wild type Receptor Protein-Tyrosine Kinases Skin Transplantation medicine.disease Hair follicle Receptors Fibroblast Growth Factor Phenotype Hypoplasia Cell biology Fibroblast Growth Factors Transplantation stomatognathic diseases medicine.anatomical_structure Endocrinology embryonic structures MESH: Skin Transplantation MESH: Hair Follicle MESH: Receptor Protein-Tyrosine Kinases Epidermis MESH: Epidermis MESH: Fibroblast Growth Factor 10 Fibroblast Growth Factor 10 Hair Follicle MESH: Fibroblast Growth Factors Signal Transduction Developmental Biology |
| Zdroj: | Development (Cambridge, England) Development (Cambridge, England), Company of Biologists, 2003, 130 (22), pp.5493-5501. ⟨10.1242/dev.00788⟩ |
| ISSN: | 1477-9129 |
| DOI: | 10.1242/dev.00788⟩ |
| Popis: | International audience; 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|