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. 2023 Feb 1;9(5):eadd9789. doi: 10.1126/sciadv.add9789

Fig. 2. FKBP12 was translocated from axonal hillock to soma and colocalized to oTau.

Fig. 2.

(A) Representative images of tau phosphorylation (CP13 antibody, red) and FKBP12 translocation in primary cortical neurons after induction of tau aggregation by oligomeric S1p fraction. Scale bars, 20 μm. (B) Representative images showed the high expression level of FKBP12 (green) in axonal hillock/axon initial segment (labeled by anti–ankyrin-G antibody, bright blue) under basal conditions whereas FKBP12 translocated to soma and dendrites when neurons bear tau aggregation. Scale bars, 20 μm. (C) Representative images showed the spatial colocalization of FKBP12 and aggregated Tau in the neurons after 24 hours of oTau seeding. Scale bars, 5 μm. DAPI, 4′,6-diamidino-2-phenylindole. (D) Quantification of FKBP12 intensity in the axon hillock of the neurons at 3 and 24 hours of S1p treatment, respectively. Data are expressed as means ± SEM. N = 10. Statistics by two-way ANOVA, post hoc multiple comparisons test by Fisher’s least significant difference (LSD). *P < 0.05, ***P < 0.005, and ****P < 0.001. (E and F) Quantification of granular intensity of CP13-labeled tau aggregates (E) and FKBP12 (F) in neurons at 3 and 24 hours of S1p treatment, respectively. Data are expressed as means ± SEM. N = 10. Statistics by two-way ANOVA, and post hoc multiple comparisons test by Fisher’s LSD. ****P < 0.001.