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Fig. 1 | Molecular Neurodegeneration

Fig. 1

From: Genetic ablation of dynactin p150Glued in postnatal neurons causes preferential degeneration of spinal motor neurons in aged mice

Fig. 1

Genetic deletion of p150Glued in Dctn1LoxP/; Cre mice. a The schematic diagram depicts the generation of Dctn1LoxP/; Cre mice in which the exon 2–4 of Dctn1 gene is deleted. b Amino acid sequence highlights residues encoded by exon 2 (light blue), exon 3 (brown), and exon 4 (navy blue). The CAP-Gly domain was marked by solid line. The basic domain was indicated by dash line. c Southern blot of genomic DNAs isolated from mouse embryonic stem (ES) cell clones shows a correct gene targeting of the Dctn1 gene locus in Dctn1+/LoxP-Frt-Neo-Frt ES cell clones. As predicted, the insertion of the LoxP-Frt-Neo-Frt gene-targeting cassette into the Dctn1 gene locus generated a new 3.8 kb BamHI fragment in Dctn1+/LoxP-Frt-Neo-Frt ES cell clones. d-e Western blot analysis shows the protein levels of p150Glued, p135+, p62, p50 and ARP1 in cultured Dctn1+/+, Dctn1+/+; Cre/Esr1, Dctn1LoxP/LoxP and Dctn1LoxP/LoxP; Cre/Esr1 cortical neurons at 7 days in vitro (DIV). Actin was used as loading control. Bar graphs show the quantification of p150Glued and p135+ levels normalized with actin (n = 3 per genotype). Data were presented as mean ± SEM. One-way ANOVA plus Tukey’s post hoc test was used for statistical analysis. ***p < 0.001 for difference against Dctn1LoxP/LoxP; Cre/Esr1, while no difference was found among Dctn1+/+, Dctn1+/+; Cre/Esr1 and Dctn1LoxP/LoxP

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