We then compared cMaf, MafB and Cxcr7 expression in E12.5 and E15.5 control (Zfhx1b heterozgyotes), Zfhx1b conditional mutants (Nkx2.1-Cre and DlxI12b-Cre) and the Dlx1/2-/- constitutive mutant (Figures 7, S2A-S2C”, S3A-S3I’). cMaf expression was nearly eliminated in all three mutants. Much of the remaining cMaf expression was in scattered blood cells and in the choroid plexus (Figure 7 H’ and H”). MafB and Cxcr7 were also greatly reduced in the SVZ of the ganglionic eminences, although they were not as strongly down-regulated as cMaf (Figures 7, S2A-S2C’, S3D-S3I’, S6D-S6I’ and S6BB-S6GG’). Therefore, Zfhx1b (and Dlx1&2) were required for cMaf, MafB and Cxcr7 expression, which are highly specific markers of immature migrating cortical interneurons (cMaf and MafB are specific for MGE-derived interneurons). Thus, the loss of cMaf, MafB and Cxcr7 expression in Zfhx1b conditional mutants (Nkx2.1-Cre and DlxI12b-Cre) provides additional evidence that cortical interneurons fail to be specified.
