Fig. 8
From: Neural defects caused by total and Wnt1-Cre mediated ablation of p120ctn in mice
Focal abnormality of β-catenin expression in the neural folds of p120fl/fl;Wnt1Cre mutant mice. Immunofluorescence of p120ctn (a, c) and β-catenin (b, d) on neural folds in the hindbrain region of a control 12–13 somite embryo (a, b) and a mutant 12–13 somite embryo (c, d). In the control embryo, β-catenin was nicely coexpressed with p120ctn (arrowheads in a, b). In the mutant embryo, both p120ctn and β-catenin were lost at the very tip of the neural folds (arrows in c, d), but the p120ctn-lacking lateral side of the neural folds retained strong β-catenin positivity (arrowheads in c, d). Scale bars: 20 μm