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The transcription factor Pax6 controls multiple aspects of forebrain development. Conditional deletion of  Pax6  in embryonic mouse cortex causes increased proliferation of cortical progenitor cells and a concomitant decrease in neural differentiation. Notch signaling regulates the balance between proliferation and differentiation of cortical progenitor cells, suggesting a possible connection between Pax6 and Notch signaling. We investigated how expression of the Notch ligand  delta-like 1  ( Dll1 ) is altered by loss of Pax6. Acute cortex-specific deletion of Pax6 resulted in a widespread decrease in the density of  Dll1 + cells at embryonic days 12.5 and 13.5 (E12.5 and E13.5). In constitutive loss-of-function mutants, decreases in the densities of  Dll1 + cells were more limited both spatially and temporally. Controlled over-expression of Pax6 had no detectable effect on  Dll1  expression. The proneural transcription factor Neurog2 is a target of Pax6 that can activate  Dll1  expression and we found clear co-expression of  Neurog2  and  Dll1  in radial glial progenitors, suggesting that Pax6’s effect on  Dll1  could be mediated through Neurog2. However, we found no change in  Dll1 + cells in  Neurog2  −/−  cortex suggesting either that Neurog2 is not directly involved, or that its loss of function in embryonic cortex can be compensated for.

Loss of Pax6 Causes Regional Changes in Dll1 Expression in Developing Cerebral Cortex