Skn-1a/Pou2f3 functions as a master regulator to generate Trpm5-expressing chemosensory cells in mice
Fig 1
Effect of Skn-1a deficiency on the functional differentiation of Trpm5-expressing brush cells in trachea.
A: Skn-1a-expressing cells were characterized using immunohistochemistry with anti-Skn-1a and anti-villin antibodies. Villin-positive brush cells were divided into two types, Skn-1a-positive (arrowhead) and Skn-1a-negative brush cells (arrow). B: Skn-1a-expressing cells were characterized by two-color in situ hybridization with RNA probes for Skn-1a and Trpm5. Skn-1a-positive brush cells were co-labeled with Trpm5 riboprobe (arrowheads). Scale bars, 20 μm. C: The impact of Skn-1a deficiency on the functional differentiation of Trpm5/Skn1a-positive brush cells in the tracheal epithelium was examined by in situ hybridization using probes for taste signaling molecules of Tas1r3, Tas2rs (Tas2r105, Tas2r108, Tas2r131), Gnat3, Plcb2 and Trpm5. The mRNA signals of taste signaling molecules observed in wild-type mice were completely absent in the Skn-1a-/- mice, indicating that Skn-1a is required for the functional differentiation of Trpm5-positive brush cells. Scale bar, 100 μm. D: The expression of taste signaling molecules (Tas1r3, Tas2r105, Tas2r108, Tas2r131, Gnat3, Plcb2, and Trpm5) in wild-type (WT) and Skn-1a-/- (KO) trachea was examined by RT-PCR. The expression of taste signaling molecule genes was not detected in Skn-1a-/- trachea. A housekeeping gene, GAPDH was used as a positive control.