Figure 3

Effect of Skn-1a deficiency on the differentiation of olfactory sensory neurons. The impact of Skn-1a deficiency on the OSN differentiation was examined by in situ hybridization using OSN neuronal marker genes Mash1 (neuronal progenitors), Ngn1 (neuronal precursors), NeuroD (differentiating/postmitotic neurons), GAP43 (immature neurons), and OMP (mature neurons) in coronal sections of wild-type and Skn-1a^-/- mice at postnatal day 7. (A) No obvious differences in the expression of marker genes were observed between Skn-1a^-/- and wild-type mice in most cases. (B) Examples of the Skn-1a^-/- mice showing a partial but obvious phenotype of a defective differentiation of OSNs only in the specific region of ectoturbinate 2 at postnatal day 7 (upper panels). Expression of GAP43 and OMP was greatly suppressed, whereas expression of Mash1, Ngn1, and NeuroD was upregulated (lower panels: high magnification images of the dotted boxes). Scale bars, 500 μm.