[P139]: Pax6 prevents premature progenitor cell differentiation, promotes the development of basal progenitors and cell‐autonomously represses ventral identities in the developing neocortex

rescued in Shh;Gli3 double mutants. We reasoned that, if Foxg1 exerts its effects on ventral telencephalon through participation in Shh-mediated antagonism of Gli3 activity, then ventral defects in Foxg1 mutants should be rescued when Gli3 activity is removed. We therefore generated Foxg1;Gli3 double mutant embryos. These showed a partial rescue of the Foxg1 mutant phenotype, in that expression of several ventral markers was restored. This suggests that Foxg1 does indeed participate in Shh-mediated antagonism of Gli3 activity. However, Foxg1;Gli3 telencephalon still exhibits several D/V patterning defects, consistent with further, Hh-independent, roles for Foxg1 in telencephalic patterning. These findings show that Foxg1 plays a central and multi-functional role in the development of the ventral telencephalon and its derivatives.