In summary, we have identified two candidate distant-acting gene regulatory elements whose activity patterns suggest that they contribute to Zfhx1b expression in the developing subpallium. These enhancer elements are activated by DLX2 in luciferase reporter assays, and are bound by DLX2 in vivo, providing strong evidence that subpallial Zfhx1b expression directly depends on Dlx1/2. Consistent with this, we observed marked alterations of Zfhx1b expression in the subpallial SVZ of Dlx1/2-deficient mice. Taken together, these results raise the possibility that the loss of Zfhx1b expression in the SVZ could contribute to the defects in differentiation and interneuron migration seen in Dlx1/2 mutants. To investigate this possibility, we compared the phenotypes of the conditional Zfhx1b and Dlx1/2-/- mutants.
