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. 2019 Sep 19;13(4):684–699. doi: 10.1016/j.stemcr.2019.08.011

Figure 5.

Figure 5

Axonal Phenotypes Caused by MT Destabilization in R406W Mutant Neurons

(A and B) Immunostaining of iPSC-derived neurons with MAP2, tau, and DAPI 30 days after dissociation (A). Arrowheads indicate neurons with tau on MAP2+ area. Scale bars, 10 μm. The percentage of tau on the dendrites was significantly increased in the mutant neurons when compared with the control neurons (B) (n = 3 independent experiments, p < 0.05; one-way ANOVA followed by Tukey's test).

(C) Immunostaining of iPSC-derived neurons with MAP2, βIII-tubulin, and tau. Scale bars, 20 μm.

(D and E) Representative immunofluorescence pictures of βIII-tubulin+ axons with (lower) or without (upper) Epothilone D (EpoD) treatment (D). Scale bars, 10 μm. There was a significantly greater number of puncta in the mutant neurons compared with control neurons, which was rescued with EpoD treatment (E) (n = 3 independent experiments). ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001 when comparing control with R406W mutants; one-way ANOVA followed by Tukey's test. #p < 0.05, ###p < 0.001 when comparing mock with EpoD; Student's t test.

Error bars indicate mean ± SEM. See also Figure S5.