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. 2017 Sep 1;144(17):3054–3065. doi: 10.1242/dev.150342

Fig. 7.

Fig. 7.

Simultaneous deletion of Shh from tongue epithelium and sensory neurons abolishes taste buds. (A) Experimental design for concurrent neural and epithelial deletion of Shh. The NST of Krt5rtTA;tetOCre;Shhflox/flox (K5-ShhcKO) mice is injected with AAV5-Cre on day 0, and mice are fed dox for 35 days. (B) In K5-AAV-ShhcKO mice, Shh is deleted in both lingual epithelium and gustatory neurons (marked by crosses). (C) Typical FFP number is significantly decreased in K5-AAV-ShhcKOs compared with control and K5-ShhcKO mice. (D) Atypical FFP number does not vary significantly across conditions, although more are evident in K5-ShhcKO mice. n=3 mice per condition. Data are mean±s.d. One-way ANOVA (C,D); **P<0.01, ***P<0.001. (E) Model for the role of Shh in taste cell renewal. Taste cell lineage progression (black arrows, left panel): New taste cells are generated from self-renewing Gli1+ progenitors (blue), which exit the cell cycle, enter buds as Shh+ precursor cells (red) and differentiate as taste cells (gray). Shh signaling in the taste progenitor niche (red dashed arrows, right panel). The niche for Gli1+ progenitors comprise both gustatory neurons and taste precursor cells expressing Shh (red). Shh ligand promotes taste cell differentiation from these Shh-responsive progenitors.