Figure 7

NFκB function is not essential for Eda signaling. A, B. E14 + 7 control SMG. C, D. E14 + 7 SMGs cultured in 100 μg/ml SN50. E, F. E14 + 7 SMGs cultured in 250 ng/ml Eda-A1 + 100 μg/ml SN50. A, C, E. Histological analysis. B, D, F. Immunolocalization of mucin protein. SN50 treatment (C, D) induces an abnormal glandular phenotype, characterized by a notable decrease in epithelial ducts and buds (b), dilated ductal lumina (*) and a marked decrease in immunodetectable mucin protein compared to controls (compare C, D to A, B). EDA treatment of SN50-treated explants (E, F) rescues the SN50-induced abnormal phenotype and restores it toward that seen in controls (compare E, F to A, B). The Eda + SN50-treated glands exhibit a marked increase in epithelial ducts and buds, more normally-appearing lumina, and a marked increase in immunodetectable mucin protein compared to glands treated with SN50 alone (compare E, F to C, D). Bar: A, C, E- 40 μm; B, D, F- 25 μm.