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Fig. 3 | Molecular Brain

Fig. 3

From: Knockdown of Son, a mouse homologue of the ZTTK syndrome gene, causes neuronal migration defects and dendritic spine abnormalities

Fig. 3

Wild-type human SON and a disease-associated mutant SON rescue migration defects induced by Son knockdown. a Schematic representations of the structures of shRNA-resistant human SON (hSONr) and disease-associated mutant SON proteins (hSONm1 and hSONm2). (b) The confirmation of shRNA resistance of various forms of human SON. HEK293 cell lysates expressing various forms of hSON with or without shRNA#1, as described above, were subjected to Western blotting with an anti-HA antibody. β-actin was used as a loading control. c Representative images showing the distribution of GFP-positive cells in the rescue experiments. The layered structure is shown as in Fig. 2c. Vectors expressing shRNA with or without those expressing various forms of hSON described in the boxes above each image were transfected into neural progenitors at E14.5. Parental pLLC vectors expressing GFP were used as a control. Coronal sections were prepared at E18.5 and stained as in Fig. 2c. d The quantification of GFP-positive cells in each layer of the developing cortex. Each layer is described as in (c). Total numbers of GFP-positive cells studied in each brain ranged 161–757. Error bars represent the SEM. n ≥ 3; *p < 0.05 by one-way ANOVA followed by Dunnett’s test. The original data are available in Additional file 1 [Table S2]

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