Next, we aimed to study whether the detected changes in Mecp2/MeCP2 expression were due to changes in cell population in response to decitabine treatment. Therefore, we studied the effect of decitabine on cell fate commitment of differentiating NSC at D2 and D8. After decitabine exposure at D2, we examined the expression of cell type-specific markers (neurons: Tub III, NeuN; astrocytes: Gfap, S100b; oligodendrocytes: Cnpase, Mbp) at the transcript levels by qRT-PCR. Comparing the control and decitabine-treated cells, we did not detect any statistically significant change in these cell type-specific genes, except for significant downregulation of Cnpase (9-fold, P <0.01) (Figure 5I). In order to determine whether any of these detected changes in transcript levels are represented in the number of cells expressing each corresponding cell type-specific marker, we performed IF experiments with specific antibodies against these markers (Figure 5J). IF experiments showed that there was no significant change in the number of TUB III+, GFAP+, CNPase+, or MBP+ cells. However, we did not find any NEUN+, or S100B+ cells in the control or decitabine-treated populations at D2, probably because these
