The fact that AD proved most competent to induce GABAergic neurons is well supported by a large body of literature25–29. For instance, both Ascl1 and Dlx2 are prominently expressed in germinal zones that produce GABAergic neurons, and ectopic expression of either factor in cortical progenitors induces markers of GABAergic neurons25,29. Ascl1 mutant mice show an aberrant development of ganglionic eminences25–28. Dlx2, in conjunction with other Dlx factors, is important for GABAergic neuron generation and migration15,27–30. The many AD expression domains during development may explain why AD induces multiple GABAergic subtypes from PSCs. However, not all neuronal subtypes generated from AD progenitors are produced from PSCs by AD expression, which suggests that additional factors may be required to generate these specific lineages.
