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Fig. 2 | Acta Neuropathologica Communications

Fig. 2

From: Impairment in dynein-mediated nuclear translocation by BICD2 C-terminal truncation leads to neuronal migration defect and human brain malformation

Fig. 2

Effects of BicD2 knockdown and mutations on neuronal cell distribution in the neocortex. a Western blot of BicD2 in primary neurons infected with lentiviruses encoding BicD2 shRNAs (shBicD2–3’U and shBicD2-CDS). BicD2 expression levels in cells infected with both shBicD2 were much lower than those infected with shCtrl. b Cell distributions in the neocortex electroporated with BicD2 shRNA and cDNA. Coronal sections of the mouse brains were collected 4 days after in utero electroporation of indicated constructs along with GFP at E14.5. While most GFP+ cells electroporated with shCtrl had already reached the CP, most cells electroporated with shBicD2-CDS and 3’U were restricted to the VZ and IZ. Expression of WT BicD2 partially rescued the migration defect. Surprisingly, expression of K775X BicD2 led to even more severe neuronal migration impairments. c Severe neuronal migration defect by the expression of K775X BicD2. Coronal sections of the mouse brains were collected 4 days after in utero electroporation of BicD2 WT, K775X or SMALED2-associated mutants (T703M and R501P) at E14. Expression of K775X, but not WT or other mutants, caused a severe defect in neuronal migration to the CP. All slices were stained with DAPI (blue) to show the cell nuclei. Bars = 100 μm. d Bar graph with individual data points showing the percentage of GFP+ cells in the CP, IZ, and VZ 4 days after electroporation (n = 3 pregnant females in each condition). Error bars represent SEM. ***P < 0.001, ****P < 0.0001. ANOVA test. Post hoc: Bonferroni test

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