Zhang, Y.Tomann, P.Andl, T.Gallant, NM.Huelsken, J.Jerchow, B.Birchmeier, W.Paus, R.Piccolo, S.Mikkola, M. L.Morrisey, E. E.Overbeek, P. A.Scheidereit, C.Millar, S. E.Schmidt-Ullrich, R.2009-09-222009-09-222009-09-22200910.1016/j.devcel.2009.05.011https://infoscience.epfl.ch/handle/20.500.14299/42770Wnt/beta-catenin and NF-kappaB signaling mechanisms provide central controls in development and disease, but how these pathways intersect is unclear. Using hair follicle induction as a model system, we show that patterning of dermal Wnt/beta-catenin signaling requires epithelial beta- catenin activity. We find that Wnt/beta-catenin signaling is absolutely required for NF-kappaB activation, and that Edar is a direct Wnt target gene. Wnt/beta-catenin signaling is initially activated independently of EDA/EDAR/NF-kappaB activity in primary hair follicle primordia. However, Eda/Edar/NF-kappaB signaling is required to refine the pattern of Wnt/beta-catenin activity, and to maintain this activity at later stages of placode development. We show that maintenance of localized expression of Wnt10b and Wnt10a requires NF-kappaB signaling, providing a molecular explanation for the latter observation, and identify Wnt10b as a direct NF-kappaB target. These data reveal a complex interplay and interdependence of Wnt/beta-catenin and EDA/EDAR/NF-kappaB signaling pathways in initiation and maintenance of primary hair follicle placodes.text::journal::journal article::research article