Figure 4.

Sox10 Induces Plasticity By Regulating fetal KIT⁺ Progenitor Maintenance and Differentiation

(A) Confocal imaging of control and Sox10^fl/fl E16 SMGs endbuds. Tissue was stained for KIT (arrow), CDH1, CCND1, K14, K5, K19, and/or K7. Scale bars, 20 μm.

(B) Graphs show fold changes in gene expression of the Fgfr2b/Kit signaling pathway in epithelial (Cdh1) cells of Sox10^fl/fl E16 SMGs, Ccnd1, heparan sulfates, as well as ductal-related markers (Krt's) and correlated signaling pathways (Egf, Wnt). Data were normalized to Rps29 and control (dotted line). Mean ± SEM, N > 3, multiple comparison t test. ^∗p < 0.05.

(C) Confocal imaging of stained E16 control and Sox10^fl/fl SMGs with ACTA2, AQP5, and K19. Arrow represents mislocated AQP5 expression in ducts. Scale bars, 20 μm.

(D) Fold changes in gene expression of proteins expressed by myoepithelial, acinar, and/or ID cells. Data was normalized to Rps29 and control (dotted line). Mean ± SEM, N > 3, multiple comparison t test. ^∗p < 0.05. ^∗∗p < 0.01.

(E) Sox10^fl/fl and control E16 SMGs were stained for SMGc, AQP5, K19, and DAPI and analyzed by confocal microscopy. Dotted line outlines the distal area. Scale bar, 20 μm.

(F) RNA sequencing data of E16 Sox10^fl/fl SMGs versus control. The list of downregulated genes was generated after bioinformatic analysis of next-generation sequencing data and cutoff at log2 fold change (FC) of −0.25. Genes outlined in bold were validated by qPCR analysis.