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How Do Taste Buds EAT?: Defining the E mbryo‐to‐ A dult T ransition in Mouse Taste Bud Development and Regeneration
Author(s) -
Barlow Linda A,
Golden Erin J,
Fellin Tim J
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.81.1
Subject(s) - taste bud , taste , sonic hedgehog , taste receptor , microbiology and biotechnology , progenitor cell , biology , embryonic stem cell , umami , population , stem cell , endocrinology , medicine , anatomy , genetics , neuroscience , signal transduction , environmental health , gene
Taste buds are collections of heterogeneous taste receptor cells (TRCs) that detect sweet, sour, salt, bitter and umami. TRCs are relatively short‐lived and continually replaced by proliferative progenitor cells situated adjacent to taste buds. In mouse embryos, taste bud precursors are first evident as small clusters of columnar epithelial cells or placodes on the developing tongue surface. Each taste placode comprises 10–20 cells that express both cytokeratin (K) 8 and the secreted protein Sonic Hedgehog (SHH). Previously we showed that SHH + placode cells differentiate into TRCs in the first postnatal week, but do not give rise to the K14 + progenitor population that supports adult TRC renewal (Thirumangalathu et al., 2009 Development). This raised the questions of how and when TRC turnover commences. Using 3D image analysis, we find that taste placode and taste bud cell number are static during embryonic development and within 1–2 days of birth, respectively; instead EdU incorporation studies and K14 genetic lineage tracing reveal that the progenitor contribution to taste buds begins by postnatal day (P) 2, steadily increasing through P14. Work from our lab and others has shown that SHH is a negative regulator of taste cell fate in embryos but paradoxically SHH promotes TRC differentiation in adults. Thus, we hypothesized that the switch in SHH function coincides with the onset of taste cell renewal. We are currently testing this idea using K14 CreER to drive SHH overexpression at specific postnatal time points. In cultured embryonic tongues, excess SHH represses formation of taste placodes, whereas in adult mice, this genetic manipulation induces formation of ectopic taste buds throughout the anterior lingual epithelium (Castillo et al., 2014 Development). Additionally we are using RNAseq analysis to identify candidate regulators of the embryo‐to‐adult transition, and more specifically to define the emerging taste bud progenitor pool in postnatal animals. Support or Funding Information Supported by R01 DC012383 to LAB and F32 DC015958 to EJG This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .