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. 2020 Oct 2;5(19):e136078. doi: 10.1172/jci.insight.136078

Figure 1. Characterization of Nna1, Ttll1, and Ttll3.

Figure 1

(A) Nna1 mRNA lacks exons 7–11 in young adult pcdSid cerebrum and cerebellum. (B) Nna1 protein is deficient in young adult pcd cerebellum, hippocampus, and substantia nigra. Dot pots with mean ± SD, n = 4–6; 2-tailed Student’s t test, compared with WT, **P < 0.01. (C) Ttll1 and Ttll3 mRNA were much higher in P20 WT PNs than in WT GNs. The Nna1 mutation reduced Ttll3 mRNA in P20 pcd. Dot pots with mean ± SD, n = 3; 2-tailed Student’s t test, compared with WT, **P < 0.01. (D) Ttll1 and Ttll3 blots were from 2 different gels. Ttll3 protein was decreased in P20 pcd cerebellum. Dot pots with mean ± SD, n = 4–6; 2-tailed Student’s t test, compared with WT, **P < 0.01. (E) Ttll1 protein (green) was equivalent in P20 WT and pcd cerebellum. Calbindin (Calb, red) in PNs, DAPI (blue) in cell nuclei. Scale bar: 50 μm. (F) Ttll3 protein (green) was decreased in P20 pcd PNs, like Calb (red) in the distal area of P20 pcd PN dendritic trees. Scale bar: 30 μm. Nna1, neuronal nuclear protein induced by axotomy; Ttll1, tubulin tyrosine ligase–like 1; pcd, Purkinje cell degeneration; PNs, Purkinje neurons; GNs, granule cell neurons.