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First published online 15 February 2006
doi: 10.1242/dev.02278

Development 133, 1045-1057 (2006)
Published by The Company of Biologists 2006
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NF-{kappa}B transmits Eda A1/EdaR signalling to activate Shh and cyclin D1 expression, and controls post-initiation hair placode down growth

Ruth Schmidt-Ullrich1,*, Desmond J. Tobin2, Diana Lenhard1, Pascal Schneider3, Ralf Paus4 and Claus Scheidereit1

1 Max-Delbrück-Center for Molecular Medicine, Robert-Rössle-Strasse 10, 13092 Berlin, Germany.
2 Medical Biosciences, School of Life Sciences, University of Bradford, Bradford BD7 1DP, UK.
3 Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, 1066 Epalinges, Switzerland.
4 Department of Dermatology, University Hospital Schleswig Holstein, Campus Lübeck, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany.

* Author for correspondence (e-mail: rschmidt{at}mdc-berlin.de)

Accepted 14 December 2005

A novel function of NF-{kappa}B in the development of most ectodermal appendages, including two types of murine pelage hair follicles, was detected in a mouse model with suppressed NF-{kappa}B activity (cI{kappa}B{alpha}{Delta}N). However, the developmental processes regulated by NF-{kappa}B in hair follicles has remained unknown. Furthermore, the similarity between the phenotypes of cI{kappa}BA{Delta}N mice and mice deficient in Eda A1 (tabby) or its receptor EdaR (downless) raised the issue of whether in vivo NF-{kappa}B regulates or is regulated by these novel TNF family members. We now demonstrate that epidermal NF-{kappa}B activity is first observed in placodes of primary guard hair follicles at day E14.5, and that in vivo NF-{kappa}B signalling is activated downstream of Eda A1 and EdaR. Importantly, ectopic signals which activate NF-{kappa}B can also stimulate guard hair placode formation, suggesting a crucial role for NF-{kappa}B in placode development. In downless and cI{kappa}B{alpha}{Delta}N mice, placodes start to develop, but rapidly abort in the absence of EdaR/NF-{kappa}B signalling. We show that NF-{kappa}B activation is essential for induction of Shh and cyclin D1 expression and subsequent placode down growth. However, cyclin D1 induction appears to be indirectly regulated by NF-{kappa}B, probably via Shh and Wnt. The strongly decreased number of hair follicles observed in cI{kappa}B{alpha}{Delta}N mice compared with tabby mice, indicates that additional signals, such as TROY, must regulate NF-{kappa}B activity in specific hair follicle subtypes.

Key words: Hair follicle, NF-{kappa}B, Eda A1, EdaR, TNF, Skin, Cyclin D1, Shh, TROY (Tnfrsf19), Mouse


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