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Fig. 7 | Acta Neuropathologica Communications

Fig. 7

From: MUNC18–1 gene abnormalities are involved in neurodevelopmental disorders through defective cortical architecture during brain development

Fig. 7

Effects of Munc18–1 knockdown on subcellular distribution of Syntaxin1A. a Localization of Syntaxin1A in Munc18–1-deficient cortical neurons. pCAG-RFP was electroporated into E14.5 cerebral cortices with pCAG-GFP-Syntaxin1A (i) or with pCAG-GFP-Syntaxin1A + sh-Munc#1 (ii, iii). Coronal sections were prepared at E18.0 and immunostained for GFP-tag (i, ii) or GFP-tag plus GM130, a Cis-Golgi marker (iii). Bars in (i-ii), 10 μm and (iii), 5 μm. b Quantification of Syntaxin1A accumulation at Golgi. The ratio of cells with GFP-Syntaxin1A accumulation in the lower CP in (a). Error bars indicate SD; Control (n = 5), Munc18–1-knockdown (n = 5); **p < 0.01 by Student’s t-test. c Quantification of subcellular localization of Syntaxin1A in migrating neurons in (a). The relative ratio of GFP-Syntaxin1A signal in perinuclear regions with high fluorescent signal to that of other regions (cytoplasm) was evaluated by ImageJ software. The criterion for “perinuclear Syntaxin1A accumulation” is high fluorescence intensity of Syntaxin1A at the perinuclear region, which was defined by ImageJ software. The fluorescent signals of GFP-Syntaxin1A at perinuclear regions and other cytoplasmic regions were calculated with ImageJ software. Error bars indicate SD of five brains containing more than 150 cells. **p < 0.01 by Student’s t-test

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