Lack of exon 10 in the murine tau gene results in mild sensorimotor defects with aging
1 Department of Public Health and Caring Sciences, Rudbeck Laboratory, Uppsala University, SE-75185 Uppsala, Sweden
2 Department of Pharmacology, Oslo University and Oslo University Hospital, Postboks 1057 Blindern, NO-0316 Oslo, Norway
BMC Neuroscience 2013, 14:148 doi:10.1186/1471-2202-14-148Published: 22 November 2013
Additional file 1: Figure S1:
A graphical illustration of the genomic structure around exon 10 on both alleles in the murine tau gene locus, tau mRNA expression and tau protein synthesis in wild-type (E10+/+, upper), E10+/- (middle) and E10-/- mice (lower). A part of the tau locus with exons 9, 11 (yellow), 10 (orange, dotted lines) and genetic deletion (►) is shown. The four microtubule domains (R1-R4) in tau protein are encoded by exons 9-12 in tau. Alternative splicing of tau in adult wild-type mouse brain results in 4R-tau protein being synthesized by both alleles (upper). Ablation of exon 10 on one of the two alleles in tau (E10+/- mice) should theoretically lead to a 1:1 balanced ratio of 3R- and 4R-tau protein synthesis (middle). This mixture of 3R-/4R-tau protein synthesis is found in adult human brain. In contrast, lack of exon 10 on both alleles in tau (E10-/-) should results in 3R-tau protein synthesis by both alleles (lower). Figure S2. Sensorimotor functions of wild-type (E10+/+), E10+/- and E10-/- mice. 13-17 months-old mice devoid of tau exon 10 (E10-/-) were also impaired in rotarod when maximum speed was recorded compared to E10+/+ (p < 0.05) and E10+/- mice (p < 0.01) (E10+/+, n = 18; E10+/-, n = 16; E10-/-; n = 15). *p < 0.05 and **p < 0.01. Figure S3. Exploratory behaviours of wild-type E10(+/+), E10+/- and E10-/- mice. At 12-16 months of age, E10+/- and E10-/- mice travelled a similar distance in the open field apparatus as wild-type mice. Figure S4. No macroscopic differences between brains of wild-type (E10+/+) and E10+/- and E10-/- mice.
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