Fig. 7: Ddx3x loss in the forebrain causes adult motor deficits.
From: Sex-specific perturbations of neuronal development caused by mutations in the autism risk gene DDX3X
A Validation of the Emx1-Ddx3x knock-out mouse line. Confocal images of a E18.5 section from an Emx1-Ddx3x-/y null mouse, showing CRE (green) exclusively in the forebrain, with corresponding loss of DDX3X (red). B Emx1-Ddx3x null pups have delayed postnatal growth. Growth curves for Emx1-Ddx3x+/+ control females (black), Emx1-Ddx3x+/- haploinsufficient females (purple), Emx1-Ddx3x+/y control males (gray), and Emx1-Ddx3x-/y null males (yellow). C Emx1-Ddx3x null males no longer display lower body weight as adults. The plot shows the body weight in adult mice across the four genotypes. D Ddx3x loss causes reduced grip in inverted screen test, when compared with Emx1-Ddx3x+/+ female and Emx1-Ddx3x+/y male controls. E, F Ddx3x loss reduces endurance in wire hanger test, as measured by latency to fall (E) and number of frames (F). G Sex and Ddx3x dosage in the forebrain affect performance on balance beam test, measured as number of frames walked. H Sex and Ddx3x dosage in the forebrain affect performance on an accelerating rotarod, measured as latency to fall. Statistics: Panels B and H, repeated measure ANOVA for the comparisons shown below the plot; Panels C, D, Kruskal–Wallis test, followed by Wilcoxon signed-rank test with Benjamini-Hochberg correction; Panels E–G, one-way ANOVA, followed by Student’s t test with Benjamini-Hochberg correction. In all panels, data were collected blind to genotype and sex; n is shown in legend as number of mice; mean ± SEM; outliers shown as ⊗; *P-value < 0.05, **P-value < 0.01, ***P-value < 0.001. Source data are provided as a Source Data file.
