Fig. 3

Myelination defects, axonal degeneration of Purkinje cells and disruption of cerebellar cortico-nuclear connection in young Tmem106b^−/− mice. a, b Western blot analysis of myelin proteins and GAPDH in 2-month-old WT and Tmem106b^−/− cerebellar lysates. Protein levels were quantified and normalized to GAPDH in b. n = 5, *, p < 0.05, **, p < 0.01, unpaired t-test. c–e Cerebellar sections from 5‐month‐old WT and Tmem106b^−/− mice were co-stained with anti-calbindin, myelin basic protein (MBP), and NF-H antibodies. MBP intensity around Purkinje cell axon and the number of giant torpedos in the axon of Purkinje cells were quantified in d and e, respectively. Scale bar = 10 µm. n = 3–4, ***, p < 0.001, unpaired t-test. f Cerebellar sections from 5‐month‐old Tmem106b^−/− mice were co-stained with anti-calbindin and Cath D antibodies. Scale bar = 10 µm. g, h Cerebellar sections from 2‐month‐old WT and Tmem106b^−/− mice were immunostained with antibodies of calbindin, synaptophysin (SYN, presynaptic marker), and MAP2. The intensity of SYN around MAP2-positive soma in the DCN region was quantified in h. Scale bar = 10 µm. n = 3, ***, p < 0.001, non-parametric test (Mann Whitney test)