Skn-1a/Pou2f3 functions as a master regulator to generate Trpm5-expressing chemosensory cells in mice
Fig 3
Impact of Skn-1a deficiency on Trpm5-positive tuft cells in digestive tracts.
A: Two-color in situ hybridization of Skn-1a (green) and Trpm5 (magenta) on sections of digestive tracts of stomach, small intestine, and large intestine of wild-type adult mice. The mRNA signals of Skn-1a were co-labeled with Trpm5 signals (arrowheads) in all tissues examined. Scale bar, 20 μm. B: Co-immunostaining using antibodies against Skn-1a (green) and villin (magenta) on sections of stomach, small intestine, and large intestine of wild-type adult mice. Skn-1a-positive cells were overlapped with villin-positive cells (arrowheads). Scale bar, 20 μm. C: The impact of Skn-1a deficiency on Trpm5-positive tuft cells was examined by double-label immunohistochemistry of Trpm5 and villin using sections of stomach, small intestine, and large intestine of wild-type (top) and Skn-1a-/- mice. Trpm5-positive cells were co-labeled with anti-villin antibody (arrowheads) in wild-type mice, whereas the expression of Trpm5 was abolished in all tested tissues in Skn-1a-/- mice. Scale bars, 20 μm. The immunoreactive signals for villin detected in wild-type mice (arrows) were not observed in Skn-1a-/- mice. D: The signals of intestinal tuft cells marker gene, Dclk1 mRNA were observed in wild-type digestive tracts, whereas no signals of Dclk1 mRNA were observed in Skn-1a-/-. Scale bars, 100 μm.