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Pathological Progression Induced by the Frontotemporal Dementia-Associated R406W Tau Mutation in Patient-Derived iPSCs

Nakamura, Mari, Shiozawa, Seiji, Tsuboi, Daisuke, Amano, Mutsuki, Watanabe, Hirotaka, Maeda, Sumihiro, Kimura, Taeko, Yoshimatsu, Sho, Kisa, Fumihiko, Karch, Celeste M., Miyasaka, Tomohiro, Takashima, Akihiko, Sahara, Naruhiko, Hisanaga, Shin-ichi, Ikeuchi, Takeshi, Kaibuchi, Kozo, Okano, Hideyuki·2019·Stem Cell Reports
DOI 10.1016/j.stemcr.2019.08.011PMC PMC6829766
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Figure 1 Generation and Characterization of iPSCs from FTD MAPT R406W Patients (A and B) Immunofluorescence for pluripotency markers alkaline phosphatase (A) and TRA-1-60 (B). Representative clones from each patient are shown. Scale bars, 500 μm. (C) Schematic diagram of the construction of targeting vectors. Top: construct of the WT targeting vector for the generation of WT lines. Bottom: construct of the mutant targeting vector for the generation of homozygous mutant lines. (D) DNA sequence of the mutation site in the heterozygous patient line (MAPTR406W/+) and in the gene-edited isogenic lines (WT line: MAPT+/+, homozygous mutant line: MAPTR406W/R406W). See also Figure S1.
Figure 1 Generation and Characterization of iPSCs from FTD MAPT R406W Patients (A and B) Immunofluorescence for pluripotency markers alkaline phosphatase (A) and TRA-1-60 (B). Representative clones from each patient are shown. Scale bars, 500 μm. (C) Schematic diagram of the construction of targeting vectors. Top: construct of the WT targeting vector for the generation of WT lines. Bottom: construct of the mutant targeting vector for the generation of homozygous mutant lines. (D) DNA sequence of the mutation site in the heterozygous patient line (MAPTR406W/+) and in the gene-edited isogenic lines (WT line: MAPT+/+, homozygous mutant line: MAPTR406W/R406W). See also Figure S1.CC BY · PubMed Central
Figure 2 Neural Differentiation of R406W iPSCs via Cerebral Organoid Dissociation (A) Schematic timeline for neuronal differentiation of iPSCs using the protocol for cerebral organoid induction. Organoids were dissociated into cortical neurons and cultured on typical two-dimensional plates. All analyses were performed after 60 days of culture. Scale bar, 500 μm (day 9, day 30), 50 μm (day 60). (B) Immunofluorescence of iPSC-derived cortical neurons using neuronal markers MAP2 and βIII-tubulin, forebrain marker TBR1, tau, and DAPI for nuclear staining. Scale bars, 50 μm. (C–G) Quantification of the percentage of cells expressing pan-neuronal markers MAP2 (C), βIII-tubulin (D), and NeuN (G), and forebrain markers TBR1 (E) and FOXG1 (F) in each iPSC-derived neuronal line (n = 3 independent experiments). (H) Quantification of the number of live cells obtained from one dissociated organoid (n = 3 independent experiments). Error bars indicate mean ± SEM.
Figure 2 Neural Differentiation of R406W iPSCs via Cerebral Organoid Dissociation (A) Schematic timeline for neuronal differentiation of iPSCs using the protocol for cerebral organoid induction. Organoids were dissociated into cortical neurons and cultured on typical two-dimensional plates. All analyses were performed after 60 days of culture. Scale bar, 500 μm (day 9, day 30), 50 μm (day 60). (B) Immunofluorescence of iPSC-derived cortical neurons using neuronal markers MAP2 and βIII-tubulin, forebrain marker TBR1, tau, and DAPI for nuclear staining. Scale bars, 50 μm. (C–G) Quantification of the percentage of cells expressing pan-neuronal markers MAP2 (C), βIII-tubulin (D), and NeuN (G), and forebrain markers TBR1 (E) and FOXG1 (F) in each iPSC-derived neuronal line (n = 3 independent experiments). (H) Quantification of the number of live cells obtained from one dissociated organoid (n = 3 independent experiments). Error bars indicate mean ± SEM.CC BY · PubMed Central
Figure 3 Reduction of Phosphorylation in R406W Mutant Tau by Multiple Kinases (A–D) Western blot analysis investigating tau phosphorylation levels at S409 (A) or T181 (C). Both pS409 and pT181 levels were significantly reduced in the R406W mutant samples (S409, B; T181, D) relative to total tau levels (K9JA) (n = 2–3 independent experiments). (E and F) Western blot analysis with pan-tau antibody Tau5 (E) revealed an increase in the ratio of 48-kDa tau (arrowhead) to total tau (both 48-kDa and 55-kDa bands) in the R406W mutant sample (F) (n = 3–4 independent experiments). (G and H) Western blot analysis investigating the effects of kinase inhibitors SB216763, KT5720, Y27632, and Roscovitine (inhibitors of GSK3β, PKA, RhoK, and CDK5, respectively) on the phosphorylation pattern of tau in WT (201B7) iPSC-derived neurons (G). Quantification of the ratio of 48-kDa tau to total tau (both 48-kDa and 55-kDa bands) revealed an increase of the ratio with SB216763 treatment, a GSK3β inhibitor, in comparison with that with the mock treatment of DMSO (H) (n = 3 independent experiments). Error bars indicate mean ± SEM. One-way ANOVA followed by Tukey's test was performed. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. See also Figures S2, S3, and S5.
Figure 3 Reduction of Phosphorylation in R406W Mutant Tau by Multiple Kinases (A–D) Western blot analysis investigating tau phosphorylation levels at S409 (A) or T181 (C). Both pS409 and pT181 levels were significantly reduced in the R406W mutant samples (S409, B; T181, D) relative to total tau levels (K9JA) (n = 2–3 independent experiments). (E and F) Western blot analysis with pan-tau antibody Tau5 (E) revealed an increase in the ratio of 48-kDa tau (arrowhead) to total tau (both 48-kDa and 55-kDa bands) in the R406W mutant sample (F) (n = 3–4 independent experiments). (G and H) Western blot analysis investigating the effects of kinase inhibitors SB216763, KT5720, Y27632, and Roscovitine (inhibitors of GSK3β, PKA, RhoK, and CDK5, respectively) on the phosphorylation pattern of tau in WT (201B7) iPSC-derived neurons (G). Quantification of the ratio of 48-kDa tau to total tau (both 48-kDa and 55-kDa bands) revealed an increase of the ratio with SB216763 treatment, a GSK3β inhibitor, in comparison with that with the mock treatment of DMSO (H) (n = 3 independent experiments). Error bars indicate mean ± SEM. One-way ANOVA followed by Tukey's test was performed. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. See also Figures S2, S3, and S5.CC BY · PubMed Central
Figure 4 Increased Cleavage of Tau by Calpain Is Dependent on the Phosphorylation State (A and B) Western blot analysis with pan-tau antibody Tau12 (A) revealed increased tau fragments ranging from 35 to 45 kDa (bracket) relative to full-length (FL) tau (brace) in the R406W mutant samples (B) (n = 3 independent experiments). (C and D) Western blot analysis of MAPTR406W/R406W samples with Tau12 when treated with 120 μM Z-VAD-FMK (pan-caspase inhibitor), 250 μM ALLN (pan-calpain inhibitor), or DMSO (mock) (C) revealed a decreased ratio of 35-kDa tau fragments (arrow) to full-length (FL) tau (brace) with calpain inhibition (D) (n = 3 independent experiments). (E and F) Western blot analysis of MAPTR406W/R406W samples with Tau5 when treated with 120 μM Z-VAD-FMK (pan-caspase inhibitor), 250 μM ALLN (pan-calpain inhibitor), or DMSO (mock) (E) revealed an increased ratio of hypophosphorylated tau (48 kDa; arrowhead) to total tau (both 48-kDa and 55-kDa bands) with calpain inhibition (F) (n = 3 independent experiments). Error bars indicate mean ± SEM. One-way ANOVA followed by Tukey's test was performed. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001. See also Figure S4.
Figure 4 Increased Cleavage of Tau by Calpain Is Dependent on the Phosphorylation State (A and B) Western blot analysis with pan-tau antibody Tau12 (A) revealed increased tau fragments ranging from 35 to 45 kDa (bracket) relative to full-length (FL) tau (brace) in the R406W mutant samples (B) (n = 3 independent experiments). (C and D) Western blot analysis of MAPTR406W/R406W samples with Tau12 when treated with 120 μM Z-VAD-FMK (pan-caspase inhibitor), 250 μM ALLN (pan-calpain inhibitor), or DMSO (mock) (C) revealed a decreased ratio of 35-kDa tau fragments (arrow) to full-length (FL) tau (brace) with calpain inhibition (D) (n = 3 independent experiments). (E and F) Western blot analysis of MAPTR406W/R406W samples with Tau5 when treated with 120 μM Z-VAD-FMK (pan-caspase inhibitor), 250 μM ALLN (pan-calpain inhibitor), or DMSO (mock) (E) revealed an increased ratio of hypophosphorylated tau (48 kDa; arrowhead) to total tau (both 48-kDa and 55-kDa bands) with calpain inhibition (F) (n = 3 independent experiments). Error bars indicate mean ± SEM. One-way ANOVA followed by Tukey's test was performed. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001. See also Figure S4.CC BY · PubMed Central
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.
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.CC BY · PubMed Central
Figure 6 Mitochondrial Transport Defects in R406W Mutant Neurons (A) Quantification of live-imaging mitochondrial trafficking revealed mitochondria in the mutant neurons (patient #2) to be less stationary and moving more in the retrograde direction, when compared with those in the control neurons (n = 3 independent experiments; ∗p < 0.05, ∗∗p < 0.01, two-way ANOVA followed by Tukey's test). (B and C) Representative pictures of fluorescent signals from iPSC-derived neurons transfected with Mito-eYFP and tdTomato, and immunostained with DAPI (C). Scale bars, 10 μm. There were fewer mitochondria on the axons of R406W mutant neurons compared with control neurons (B) (n = 3 independent experiments; ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001, one-way ANOVA followed by Tukey's test), which recovered to the control level with EpoD treatment (n = 3 independent experiments; #p < 0.05, ##p < 0.01, ###p < 0.001, Student's t test). Error bars indicate mean ± SEM.
Figure 6 Mitochondrial Transport Defects in R406W Mutant Neurons (A) Quantification of live-imaging mitochondrial trafficking revealed mitochondria in the mutant neurons (patient #2) to be less stationary and moving more in the retrograde direction, when compared with those in the control neurons (n = 3 independent experiments; ∗p < 0.05, ∗∗p < 0.01, two-way ANOVA followed by Tukey's test). (B and C) Representative pictures of fluorescent signals from iPSC-derived neurons transfected with Mito-eYFP and tdTomato, and immunostained with DAPI (C). Scale bars, 10 μm. There were fewer mitochondria on the axons of R406W mutant neurons compared with control neurons (B) (n = 3 independent experiments; ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001, one-way ANOVA followed by Tukey's test), which recovered to the control level with EpoD treatment (n = 3 independent experiments; #p < 0.05, ##p < 0.01, ###p < 0.001, Student's t test). Error bars indicate mean ± SEM.CC BY · PubMed Central

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Metadata

Authors
Nakamura, M., Shiozawa, S., Tsuboi, D., Amano, M., Watanabe, H., Maeda, S., Kimura, T., Yoshimatsu, S., Kisa, F., Karch, C. M., Miyasaka, T., Takashima, A., Sahara, N., Hisanaga, S.-I., Ikeuchi, T., Kaibuchi, K., & Okano, H.
Venue
Stem Cell Reports
Publisher
Elsevier BV
Published
2019-10
Volume
13
Issue
4
Pages
684-699
ISSN
2213-6711
DOI
10.1016/j.stemcr.2019.08.011
PMC
PMC6829766
Cited by
76
References
8
Language
en
Licence
Funders
  • Japan Agency for Medical Research and Development
  • Foundation for the National Institutes of Health
  • Ministry of Education, Culture, Sports, Science and Technology

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