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Fig. 3 | BMC Developmental Biology

Fig. 3

From: Neural defects caused by total and Wnt1-Cre mediated ablation of p120ctn in mice

Fig. 3

Conditional ablation of the mouse p120ctn encoding gene by the action of Wnt1-Cre results in neural tube defects (NTDs). Control mice carried two floxed p120ctn encoding alleles (p120ctnfl/fl) but lacked the Wnt1-Cre gene; mutant p120ctnfl/fl;Wnt1Cre mice had ablated p120ctn encoding alleles at sites of Wnt1Cre expression. a, b Lateral views at E9.5 of a control embryo (a), and a mutant embyo, the latter displaying a NTD (b, arrow). c-f Coronal sections at the level of the hindbrain of an E9.5 control mouse (c, e) and an E9.5 mutant mouse (d, f) were stained with either DAPI (c, d) or with anti-p120ctn antibody (e, f). Arrows in (c, e) point at normal, almost closed p120ctn-positive neural folds. Arrows in (d, f) point at extended unfolded p120ctn-lacking neural folds. Scale bars: 20 μm. g-j External lateral (g, h) and dorsal (I, j) views of E11.5 head structures. Control embryos (g, i) show normal brain development (mb, midbrain; me, metencephalon; my, myelencephalon). Mutant embryos show exencephaly (h, arrow), expanded mb and me structures and non-closure of the neural tube (j, black arrow). k, l IHC of p120ctn in sagittal sections of the head region of E13.5 embryos. There is ubiquitous expression in the control embryo (k), but an obvious lack of p120ctn expression in the enlarged hindbrain region and the facial structures of the mutant embryo (l, arrows)

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