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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

From: Loss of Tmem106b is unable to ameliorate frontotemporal dementia-like phenotypes in an AAV mouse model of C9ORF72-repeat induced toxicity

Fig. 1

Generation of mice with targeted Tmem106b gene disruption. a Genomic structure of the wild-type mouse Tmem106b allele and the gene trap vector used to target the mouse Tmem106b gene. Rectangular boxes represent exons that are shaded in gray or white to denote coding and non-coding exons, respectively. White arrowheads signify Flp recombination target (FRT) sites and black arrowheads represent loci of crossover in P1 (LoxP) sites. Genotyping primer binding sites are labeled and denoted with black arrows above each genomic structure. b PCR analysis of DNA obtained from the hair follicles of Tmem106b wild-type (+/+), heterozygous (+/−), or knockout (−/−) mice using the primers depicted in panel a. c Quantitative PCR analysis measuring Tmem106b mRNA levels in Tmem106b +/+, +/−, and −/− mouse brain (n = 4 per genotype) at 3 months of age. The graph represents the mean ± S.E.M.; ****p < 0.0001 by one-way ANOVA followed by a Fisher’s LSD post-hoc test. d Western blot depicting Tmem106b protein levels (black arrowhead) in 3-month-old Tmem106b +/+, +/−, and −/− mouse brain tissue. Gapdh was used as a loading control. e Quantification of Tmem106b protein levels in Tmem106b +/+, +/-, and -/- mouse brain at 3 months of age (n =3 per genotype)

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