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Development ePress online publication date 15 Feb 2006
doi: 10.1242/dev.02278

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Research article

(2006)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-Ullrich*, Desmond J. Tobin, Diana Lenhard, Pascal Schneider, Ralf Paus, and Claus Scheidereit
* Author for correspondence (e-mail: rschmidt{at}mdc-berlin.de)

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.
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