Figure 6: β-Catenin regulates the expression and location of aPKC through Tcf-dependent and -independent mechanisms. | Nature Communications

Figure 6: β-Catenin regulates the expression and location of aPKC through Tcf-dependent and -independent mechanisms.

From: Sustained Wnt/β-catenin signalling causes neuroepithelial aberrations through the accumulation of aPKC at the apical pole

Figure 6

(a) HH-12 chicken neural tubes were electroporated with control (pCIG), β-cateninS33Y, Vp16·Tcf3 or both and analysed 48 h later. The distance from the roof to the floorplate was measured at the apical (apical distance) and basal (basal distance) faces of the epithelium, and the ratio between them was plotted. For each treatment, four sections from each of four embryos were measured. (b) Vp16·Tcf3-transfected sections were stained after 48 h with antibodies against GFP (blue, transfection), aPKC, β-catenin or ZO-1 (red) and N-cadherin (green). Arrowheads indicate groups of cells in the ventricle and the arrows Vp16·Tcf3+ cells with cytoplasmic accumulations of aPKC. (c) The aPKCı and aPKCζ mRNAs were measured by real-time PCR in chicken neural tubes 48 h after transfection with control (pCIG), β-cateninS33Y or Vp16·Tcf3, five embryos per data point were pooled. The bar graphs show the mean±s.d. of three experiments. Significant differences were tested by one-way analysis of variance (ANOVA) followed by the Tukey’s test. (d) Chicken neural tubes were stained with antibodies against GFP (blue, transfection), aPKC (red) and N-cadherin (green) 48 h after electroporation with Vp16·Tcf3 or Vp16·Tcf3 plus β-cateninS33Y. The right panel shows enlarged images of three more examples of the effect of control or β-cateninS33Y expression on the distribution of aPKC, these pictures are displayed in grey scale for better comparison. Scale bar represents 50 μm in b,d (left) and 25 μm in d (right).

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