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. 2009 Aug 14;5(8):e1000600. doi: 10.1371/journal.pgen.1000600

Figure 2. Loss of MBNL1 enhances rotarod deficits in SCA8 BAC-EXP5 mice.

Figure 2

(A) Line plot of average latency to fall in seconds over four consecutive trial days. Individual trial day data points are the average of the last 3 trials and show a decreased latency for SCA8+/−; Mbnl1 +/ΔE3 mice that is significantly different from WT at day four. (B) Bar graph shows the mean latency to fall (Sec) for non-transgenic, singly transgenic SCA8 BAC-EXP5 (SCA8+/−). heterozygous Mbnl1 knock-out (Mbnl1+ /ΔE3) and doubly transgenic SCA8 BAC-EXP5; Mbnl1 +/ΔE3 (SCA8+/−; Mbnl1 +/ΔE3; n = 17) littermates. As previously reported for this low-copy line (SCA8 BAC-EXP5), no significant difference between non-transgenic littermates and singly transgenic SCA8+/− animals was found. Although singly transgenic Mbnl1+ /ΔE3 mice show a significant decrease in latency compared to non-transgenic (p = 0.01), doubly mutant SCA8+/−; Mbnl1+ /ΔE3 perform significantly worse than both WT and singly mutant Mbnl1+ /ΔE3 animals (p = 0.003). *and ‡ = significant differences between groups.