Fig. 7
From: Neural defects caused by total and Wnt1-Cre mediated ablation of p120ctn in mice
Focal abnormalities of E-cadherin expression in non-neural ectoderm of p120fl/fl;Wnt1Cre mutant mice. a-h IHC of p120ctn (top panels) and E-cadherin (bottom panels) on neural folds/tube in the hindbrain region of control and mutant embryos. Detection was on a 12–13 somite control embryo with open neural folds (a, b), on a 12–13 somite control embryo with closed neural tube (c, d), on a 12–13 somite mutant embryo with open neural folds (e, f), and on an 18–22 somite mutant embryo with NTD (g, h). The mutant embryos showed the expected loss of p120ctn (arrows in e, g). In b-h, the respective ends of the E-cadherin-positive non-neural ectoderm flanking the neural folds/tube are indicated by arrowheads. i-k Immunofluorescence of E-cadherin (nuclear counterstaining by DAPI) in the hindbrain region of either 12–13 somite control embryos with open neural folds (i) or a closed neural tube (j), or a 12–13 somite mutant embryo with open neural folds (k). Arrows indicate the very tip of the neural fold (i, k) or the dorsal closure point of the neural tube (j). There is an E-cadherin deficiency at the very tip of the neural folds of the mutant embryo (k, arrow). Scale bars: 20 μm