Figure 5: Wdfy3^lacZ/lacZ mice generated through gene targeting exhibit more severe neurodevelopmental defects than Wdfy3^disc/disc mice.

(a) Nissl-stained coronal hemisections through the forebrains of WT, heterozygous and homozygous lacZ newborn pups illustrate the malformations present in affected mutants. The yellow dashed line indicates the cortical length in the WT as measured from the corticostriatal boundary to the ventricular apex. The red dashed line indicates differences in cortical length present in the lacZ mutants. (b) Close-ups of cortical segments of lateral and dorsal positions demonstrate cortical thinning in lacZ mutants. (c) Bar diagrams showing the results (mean and s.e.m.) of statistical analysis (Student’s t-test) for compared morphological parameters. Number (n) of analysed pups and calculated P values of significant changes (asterisks) are indicated in the bar diagrams. Measurements were taken as shown in Fig. 1e. (d) Analysis of β-gal expression in Wdfy3^lacZ mice labels Wdfy3⁺ cells and their progeny and confirms at E11.5 dispersed β-gal⁺ cells in the VZ, MZ and meninges (Me). (e) Coronal sections of P0 dorsomedial somatosensory cortex labeled for β-gal expression and immunohistochemically for NeuN and glial fibrillary acidic protein (GFAP) confirms that Wdfy3⁺ progenitors contribute to many neurons and some glia (green arrowheads) but not all NeuN⁺ or GFAP⁺ cells (red arrowheads). Scale bar in a is 500 μm, in b 200 μm, in d 50 μm and in e 20 μm.