Abstract
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.
Highlights
The sense of taste is indispensable for feeding behavior
As Krt14+ basal cells give rise to both lingual epithelium and taste bud cells [6], and Krt5 and Krt14 are co-expressed by lingual basal keratinocytes [6, 33], we first confirmed that our doxycycline-mediated Krt5-driven induction system results in Cre-mediated reporter expression in basal keratinocytes, lingual epithelium and taste bud daughter cells
Following 4 days of dox feeding of adult mice, the majority of epithelial cells around taste buds were Xgal+ in the posterior circumvallate papilla (CVP) and anterior fungiform papillae (FFP), while only a few Xgal+ cells were detected within taste buds (S1A2 and S1B2 Fig, white arrowheads)
Summary
The sense of taste is indispensable for feeding behavior. It informs the body whether food is harmful or nutritious, and is critical for regulating the intake of essential nutrients. Regardless of location, each taste bud is a heterogeneous collection of ~60–100 elongate cells, which have both neural and epithelial characteristics: neural in that they transduce chemical signals, i.e., salt, sour, sweet, bitter, and umami (savory), into electrochemical signals which are transmitted via sensory afferents to the brain [1]; and epithelial, given their morphology and embryonic origin [2, 3](but see [4]) and the fact that taste cells are continuously renewed throughout life [5]. The Krt14+ progenitor population produces the non-taste or general epithelium, within which taste buds are embedded, and these cells undergo progressive differentiation, mirroring that of skin, to form the keratinized lingual epithelium [7]. In order to maintain the sense of taste, the Krt14+ progenitor population must: (1) produce both rapidly renewing, short-lived non-taste epithelium, and more slowly renewing, longer lived taste bud cells; and (2) generate the proper ratio of taste cell types I, II and III within each bud. We have a limited understanding of how cell fate decisions are regulated within the lingual epithelial progenitor population
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