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Chunk #16 — Results — MGE-Derived Pallial Interneurons Migrate to the Striatum When Deleting Zfhx1b in the VZ of the MGE Using Nkx2.1-Cre

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Dlx1&2-dependent expression of Zfhx1b (Sip1, Zeb2) regulates the fate switch between cortical and striatal interneurons.
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To distinguish whether the abnormal collections of cells in the mutant striatum were cortical or striatal interneurons, we examined expression of Cxcr7 and NPY. At E15.5 Cxcr7 marked migrating cortical interneurons, and few cells in the striatum (Figures 7J,7K and 7L), suggesting that it is a relatively specific cortical interneuron marker (Wang et al., 2011). In the mutant, there was a robust reduction of Cxcr7 expression in the pattern of migrating cortical interneurons, without a substantive increase in striatal expression (Figures 7J’,7K’,7L’); a similar result was seen for Cux2 (not shown). On the other hand, at E15.5, NPY expression strongly marks scattered striatal cells (probably interneurons), and relatively few migrating cortical interneurons (note, most of the cortical expression at this age resembles that of immature projection neurons in the cortical plate). In the mutant, there was a robust increase in NPY expression in the striatum (Figures 2P-2R’), in a pattern closely resembling the pattern of ectopic Nkx2-1, Lhx6 and Sox6 (Figures 2D-2L’). Thus, we propose that the mutant cortical interneurons are transformed towards GABAergic striatal interneurons.