Figure 2. MCT8-Deficient Cells Have Normal Differentiation and T₃-Dependent Neuronal Maturation.

(A) Quantifying immunocytochemistry-stained cells showed that MCT8-deficient and control iPSCs had similar neural differentiation potential into Nestin+ progenitor cells, GFAP+ astrocytes and βIII-Tubulin+ neurons. Error bars represent SD.

(B) Scheme for differentiating iPSCs into neural cultures, in the presence or absence of T₃ (100 nM) throughout 30–40 days.

(C) Mean of total spikes/5 min in the MCT8 intact (control) CS02iCTR, CS03iCTR and CS01iMCT8^cor lines differentiated in the presence of T₃ (solid line) was significantly higher than in the absence of T₃ (dashed line) (ANOVA, n = 3, p < 0.0384).

(D) Mean of total spikes/5 min in the CS01iMCT8, CS58iMCT8 and CS03iCTR^mut MCT8-deficient lines differentiated in the presence of T₃ (solid line) was significantly higher than in the absence of T₃ (dashed line) (ANOVA, n = 3, p < 0.014).

(E) Mean of total bursts/5 min in the MCT8 intact (control) lines in the presence of T₃ (solid line) was significantly higher than in the absence of T₃ on the third week of differentiation (t test, n = 3, p < 0.01).

(F) Mean of total bursts/5 min in the MCT8-deficient lines in the presence of T₃ (solid line) was not significantly higher than in the absence of T₃ (dashed line).

(G) Volcano plot shows differences of expression patterns in healthy control cells in response to T₃ treatment. The dotted lines represent 1.5-fold differentially expressed genes by paired Student’s t test followed by Benjamini Hochberg correction for multiple comparisons at a false discovery rate (FDR) of 0.1. See Tables S3 and S4 for complete list.

See also Figure S4 and Tables S3 and S4.