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Fig. 2. Neurogenesis and cell proliferation in the cerebral cortex of mice harboring mutations in the distinct DNA-binding domains of Pax6. (A-E) Micrographs show coronal sections of the lateral cerebral cortex immunostained for NeuN (red) (neuronal marker) and PH3 (green) (marker for cells in M-phase) at embryonic day (E)14 in the respective mouse mutants as indicated in the panels. Note that the band of NeuN-positive cells is reduced in the PD mutant Pax6^Aey18–/– (B) compared to WT cortex (A), indicating a reduced neurogenesis that appears comparable in extent to the phenotype in the functional null Pax6^Sey–/– (E). In contrast, no such changes could be observed for the cortex of Pax6(5a)–/– (C) or the HD-mutant Pax6^4Neu–/– (D). In the mutants with an impaired neurogenesis (the PD mutant Pax6^Aey18–/– and Pax6^Sey–/–), we observed an increase in precursors (green PH3-positive cells in B,E), while no changes in comparison to WT (A) were seen in the cortex of Pax6(5a)–/– (C) and Pax6^4Neu–/– (D). Note that the PH3-positive cells were mostly increased in the subventricular zone (SVZ, arrowhead in A; increase in B and E), but not in the VZ (arrow in A). Thus, the PD of Pax6 is necessary and sufficient to mediate the effects of Pax6 on neurogenesis and cell proliferation in the cerebral cortex, while targets of the HD seem to play no role in these aspects. The dashed white line (A-E) indicates the ventricular surface of the cortex. MZ, marginal zone; CP, cortical plate; SVZ, subventricular zone; VZ, ventricular zone; CTX, cortex; GE, ganglionic eminence. Scale bar: 100 µm.

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