Fig. 6
From: Neural defects caused by total and Wnt1-Cre mediated ablation of p120ctn in mice
Focal abnormalities of N-cadherin expression in the neural folds of p120fl/fl;Wnt1Cre mutant mice. a-h Immunofluorescence of p120ctn (left panels) and N-cadherin (right panels; nuclear counterstaining by DAPI) on neural folds/tube in the hindbrain region of young embryos (lateral sides of folds are annotated by arrowheads). Detection was on 8-somite (a, b) and 12-somite (e, f) control embryos, and on 10-somite (c, d) and 12-somite (g, h) mutant embryos. The mutant embryos showed focal loss of both p120ctn and N-cadherin at the very tip of the neural folds (arrows in c, d, g, h), but in the 12-somite mutant embryo the p120ctn-lacking lateral side of the neural folds retained strong N-cadherin positivity (arrowheads in g, h). Scale bar: 20 μm. i-q IHC of p120ctn (i-k) and of N-cadherin (l-n) on neural folds/tube in the hindbrain region of 18–22 somite embryos. Scale bars: 20 μm. o-q Immunofluorescence of N-cadherin in areas, corresponding to the squares in panels l-n. The embryos analysed were control (i, l, o), mutant with closed neural tube (j, m, p) and mutant with NTD (k, n, q). p120ctn-lacking neural folds/tube (arrows in j, k) retained N-cadherin positivity (m, n, p, q) although N-cadherin was locally aggregated in case of NTD (n, arrows in q)