Skip to main content
. 2020 Aug 31;11:4363. doi: 10.1038/s41467-020-18175-4

Fig. 1. Adherens junction disruption induces ectopic accumulation of PAX6-positive cells.

Fig. 1

High-power fluorescent micrographs of the ventricular zone (VZ) show the adherens junction belt (white arrowheads) around the ventricle (V). ΔnCdh2-GFP- (b, d), but not control GFP- in utero electroporation (IUE) (a, c), demolishes adherens junctions (open arrowheads). e–j Laminin (LAMA1)-immunostaining of the developing cerebral cortex from GFP- and ΔnCdh2-GFP-electroporated embryos. High-power images (g, j) demonstrate that the attachment of the basal endfeet of RGPCs to the pial surface is not affected directly by the disruption of cadherin-based adherens junctions at the ventricular surface. k Selective damage of the apical adherens junction does not affect the two main morphological types of radial glia endfeet at the basal surface (two-sided Student’s unpaired t test, P = 0.951; n = 43 sections from n = 3 animals per GFP treatment, n = 37 sections from n = 3 animals per ΔnCdh2-GFP-treatment). Graphs show box-and-whisker plots (including minima, maxima and median values, lower and upper quartiles) with single values. l–o Breakdown of adherens junctions prompts delamination (g–h) and ectopic accumulation of PAX6-positive cells in the subventricular zone. p Distribution of PAX6-positive cells in five equal bins (Roman numerals) (two-sided Mann–Whitney U test for all comparisons; 4th bin ***P = 0.0004 and 5th bin ***P = 0.0003; n = 13 sections from n = 3 animals per GFP treatment; n = 11 sections from n = 3 animals per ΔnCdh2-GFP-treatment). Data are shown as median (line) and interquartile range (transparent band). Scale bars: a–d, l–o: 50 μm, e–j: 25 μm. Source data are provided as a Source Data file.