Fungiform taste papillae form a regular array on the dorsal tongue. Taste buds arise from papilla epithelium¹ and, unusually for epithelial derivatives, synapse with neurons, release neurotransmitters and generate receptor and action potentials^{2, 3}. Despite the importance of taste as one of our five senses, genetic analyses of taste papilla and bud development are lacking. We demonstrate that Wnt--catenin signaling is activated in developing fungiform placodes and taste bud cells. A dominant stabilizing mutation of epithelial -catenin causes massive overproduction of enlarged fungiform papillae and taste buds. Likewise, genetic deletion of epithelial -catenin or inhibition of Wnt--catenin signaling by ectopic dickkopf1 (Dkk1)^{4, 5, 6} blocks initiation of fungiform papilla morphogenesis. Ectopic papillae are innervated in the stabilizing -catenin mutant, whereas ectopic Dkk1 causes absence of lingual epithelial innervation. Thus, Wnt--catenin signaling is critical for fungiform papilla and taste bud development. Altered regulation of this pathway may underlie evolutionary changes in taste papilla patterning.

1. Departments of Dermatology and Cell and Developmental Biology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
2. Department of Cell and Developmental Biology, University of Colorado Health Sciences Center, Aurora, Colorado 80045, USA.
3. Department of Dermatology, University of Michigan, Ann Arbor, Michigan 48109, USA.
4. Department of Pharmacology, Howard Hughes Medical Institute and Institute for Stem Cell and Regenerative Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA.
5. Department of Pharmacology, Graduate School of Medicine, Kyoto University, Yoshida-Konoé-cho, Sakyo, Kyoto 606–8501, Japan.
6. These authors contributed equally to this work.

Correspondence to: Sarah E Millar¹ e-mail: millars@mail.med.upenn.edu

Correspondence to: Linda A Barlow² e-mail: Linda.Barlow@uchsc.edu

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