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. Author manuscript; available in PMC: 2013 Mar 20.
Published in final edited form as: Neuron. 2012 Sep 20;75(6):1067–1080. doi: 10.1016/j.neuron.2012.07.009

Fig. 1. Generation of Elavl3-/- knockout mice.

Fig. 1

(A) The targeting construct used in generating elavl3 KO locus by homologous recombination. (B) The expression of Elavl3 protein is abolished in Elavl3-/- brain tissue (P21 WT, heterozygote and KO mice (littermates), as indicated). The lower heavy band corresponds to Elavl3, upper bands represent Elavl2 and Elavl4. Results from P21 WT, Elavl3+/- and Elavl3-/- mice were repeated in 3 independent litters. (C) Rotarod or hotplate testing of cerebellar or sensory physiology in Elavl3+/- or -/- littermates, as indicated; second until falling off the rod or tail twitch are shown. Rotarod testing was done with 6~8 week-old males (n=3; p < 0.0001), and hotplate testing was done with 7~9 week-old males (n=3, p = 0.11). (D-E) IF microscopy of Elavl3-/- mice compared to WT (+/+) littermate controls. A pan anti-nElavl antibody (α-nElavl) was used for IF, and contrasted with staining for the Purkinje neuronal marker Calbindin (D) or nuclei (DAPI, (E)). (E) Arrows point to nElavl immunostaining in WT and lack of it in Elavl3-/- DG.