| Taste buds consist of 60–100 fusiform cells, including 3 differentiated types: I, II, III, and basal cells (IV). Homeostasis of taste buds is maintained by continual addition of new cells from taste progenitors located outside taste buds, balanced by regular taste cell loss via apoptosis. In mammals, lingual taste buds are located in 3 types of taste papillae: anteriorly are the fungiform (FFP), while foliate and circumvallate (CVP) are located posteriorly. For my thesis work, I investigated taste cell renewal under normal conditions, and in response to irradiation injury. To assess its potential functions in taste cell renewal, I first described expression of the morphogen, BMP4, in mice carrying one allele of BMP4-LacZ BMP4 expression in CVP and FFP is both similar and different. In CVP, BMP4 is expressed exclusively by cells in taste buds, which likely are immature taste cells. In both CVP and FFP, however, BMP4-expressing cells are located in the taste progenitor region outside of taste buds, i.e., perigemmaly. These perigemmal BMP4 cells appear to be mitotically silent, suggesting that they are slow cycling stem cells, or comprise the stem cell niche which in turn regulates taste cell renewal. Next, I analyzed how taste cell renewal changes following irradiation by treating mice with γ-irradiation to the head and neck. I found that irradiation targets the taste progenitor pool; these cells temporarily cease dividing, and some undergo apoptosis. This results in a transient reduced influx of new cells into taste buds. Taste receptor cells only became significantly reduced in number well after taste progenitors resumed proliferation, suggesting that later loss of taste cells following irradiation was due to continued normal cell death, paired with temporary interruption of cell replacement. Finally, I tested if the effects of radiation on taste epithelium are mitigated in Protein kinase C delta (PKCδ) null mice. My initial results reveal that the dramatic reduction in proliferative index observed immediately following irradiation in taste epithelia of wild type mice is mitigated significantly in PKCδ null mice, suggesting that PKCδ is required for apoptotic cell death and/or cell cycle arrest in irradiated taste epithelium. |
