β-Catenin Signaling Biases Multipotent Lingual Epithelial Progenitors to Differentiate and Acquire Specific Taste Cell Fates.

摘要: Continuous taste bud cell renewal is essential to maintain function in adults; however, the molecular mechanisms that regulate turnover are unknown. Using inducible Cre-lox technology, we show activation of β-catenin signaling multipotent lingual epithelial progenitors outside buds diverts daughter cells from a general fate. Moreover, while comprise 3 morphological types, drives overproduction primarily glial-like Type I both anterior fungiform (FF) and posterior circumvallate (CV) buds, with small increase II receptor for sweet, bitter umami, but does not alter III sour detector cells. Beta-catenin post-mitotic precursors likewise regulates differentiation; forced these Shh+ promotes fate FF CV likely so non-cell autonomously. Our data consistent model where levels within dictate prior or during entry new into buds; high induces cells, intermediate drive differentiation, low may differentiation