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PMID:14597196
| Citation |
Ellis, T, Smyth, I, Riley, E, Bowles, J, Adolphe, C, Rothnagel, JA, Wicking, C and Wainwright, BJ (2003) Overexpression of Sonic Hedgehog suppresses embryonic hair follicle morphogenesis. Dev. Biol. 263:203-15 |
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| Abstract |
The Sonic Hedgehog (Shh) signalling pathway plays a central role in the development of the skin and hair follicle and is a major determinant of skin tumorigenesis, most notably of basal cell carcinoma (BCC). Various mouse models involving either ablation or overexpression of key members of the Shh signalling pathway display a range of skin tumours. To further examine the role of Shh in skin development, we have overexpressed Shh in a subset of interfollicular basal cells from 12.5 dpc under the control of the human keratin 1 (HK1) promoter. The HK1-Shh transgenic mice display a range of skin anomalies, including highly pigmented inguinal lesions and regions of alopecia. The most striking hair follicle phenotype is a suppression in embryonic follicle development between 14.0 and 19.0 dpc, resulting in a complete absence of guard, awl, and auchene hair fibres. These data indicate that alternative signals are responsible for the development of different hair follicles and point to a major role of Shh signalling in the morphogenesis of guard, awl, and auchene hair fibres. Through a comparison with other mouse models, the characteristics of the HK1-Shh transgenic mice suggest that the precise timing and site of Shh expression are key in dictating the resultant skin and tumour phenotype. |
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| Keywords |
Animals; Carcinoma, Basal Cell/etiology; Cell Division; Cytoskeletal Proteins/analysis; Hair Follicle/embryology; Hedgehog Proteins; Homeostasis; Keratins/genetics; Mice; Mice, Transgenic; Morphogenesis; Skin Neoplasms/etiology; Trans-Activators/analysis; Trans-Activators/genetics; Trans-Activators/physiology; beta Catenin |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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