to levels comparable to those of the unaffected control (Figure 7D–H). Moreover, GAD1+ cells at TD31 were not aberrantly entering the cell cycle, suggesting that GABAergic neurons were terminally differentiated in the organoids (Figure S 6C, D). Taken together, these data suggest that the early increase in proliferation of GABAergic neuronal progenitor cells in proband-derived organoids gave rise to an increased proportion of mature GABAergic interneurons, and that FOXG1 RNAi restored both these early and late effects to levels comparable to those found in unaffected family members. Similar experiments revealed smaller or non-significant changes in the proliferation of PAX6+ and TBR1+ precursor cells after FOXG1 RNAi (Figure S7), suggesting that upregulated FOXG1 expression in ASD neural cells was driving an early proliferative effect in neuronal precursor cells of the GABAergic lineage.
