Zfhx1b was required to generate GABAergic cells that migrate to the cortex, and to repress the generation GABAergic cells that migrate to the striatum. We suggest that Zfhx1b promotes a fate switch between cortical interneurons and nNos/NPY/Sst striatal interneurons through repression of Nkx2-1 expression. Furthermore, Zfhx1b mutants have reduced striatal PV interneurons (Figure 4M,4M’); thus, Zfhx1b could also control this fate decision. Zfhx1b is required in the MGE SVZ, and not the VZ, to promote the specification of pallial interneurons, as we observed largely the same phenotype using DlxI12b-Cre (SVZ recombination, Figures 3, S1, S3) and Nkx2.1-Cre (VZ recombination; Figures 1, 2, S1, S2).
