Fig. 5: The neurogenesis defects in the patient-derived organoids are due to suppressed AKT and ERK. | Cell Death & Disease

Fig. 5: The neurogenesis defects in the patient-derived organoids are due to suppressed AKT and ERK.

From: CUL4B mutations impair human cortical neurogenesis through PP2A-dependent inhibition of AKT and ERK

Fig. 5

A Western blots showing the expression of the indicated proteins in organoids. B Western blots showing phosphorylation of ERK and AKT in the isogenic control (Correct) or the patient-derived (Patient) organoids with the indicated treatment. The number below each band is the normalized ratio between the intensity of the band and the intensity of GAPDH band from the same sample. C Ki67 staining (green) of the indicated organoids at 48 h after EdU labeling (red). Scale bar, 50 μm. N = 8. D PAX6 and TUJ1 staining in the indicated organoids on day 35. The bar graphs show the thickness (N = 12-18) and the area (N = 12-14) of the PAX6+ layers in organoids. E CTIP2 and TBR2 staining in day-50 organoids. Scale bar, 50 μm. The bar graphs show the proportion of TBR2+ cells (N = 10) and the proportion of CTIP2+ cells (N = 10). F SATB2 and MAP2 staining in day-60 organoids. Scale bar, 50 μm. The bar graph shows the proportion of SATB2+ cells. N = 8. Data are presented as the mean ± SEM. The statistical significance was determined using two-tailed unpaired t-test. *P < 0.05; **P < 0.01; ***P < 0.001. ns: no significance.

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