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

Continuous taste bud cell renewal is essential to maintain taste function in adults; however,the molecular mechanisms that regulate taste cell turnover are unknown. using inducible cre-lox technology,we show that activation of β-catenin signaling in multipotent lingual epithelial progenitors outside of taste buds diverts daughter cells from a general epithelial to a taste bud fate. moreover,while taste buds comprise 3 morphological types,β-catenin activation drives overproduction of primarily glial-like type i taste cells in both anterior fungiform (ff) and posterior circumvallate (cv) taste buds,with a small increase in type ii receptor cells for sweet,bitter and umami,but does not alter type iii sour detector cells. beta-catenin activation in post-mitotic taste bud precursors likewise regulates cell differentiation; forced activation of β-catenin in these shh+ cells promotes type i cell fate in both ff and cv taste buds,but likely does so non-cell autonomously. our data are consistent with a model where β-catenin signaling levels within lingual epithelial progenitors dictate cell fate prior to or during entry of new cells into taste buds; high signaling induces type i cells,intermediate levels drive type ii cell differentiation,while low levels may drive differentiation of type iii cells. © 2015 gaillard et al.