Figure 5.

Control of neocortical projection neuron fate by Fezf2. A: In wildtype mice Fezf2 is expressed at high levels in L5 SCPNs that send axons to the midbrain, hindbrain and spinal cord and at lower levels in CThPNs that project to the thalamus. Fezf2^−/− mice fail to generate subcerebral projections, and instead increased projections to the thalamus are observed. In the absence of Fezf2, L5 neurons extend axons across the corpus callosum, similar to CPNs. B: Gene expression changes after loss of Fezf2 suggest that it represses alternate CPN and CThPN fates. C: A model of the genetic interactions involving Fezf2 during generation of distinct cortical projection neuron subtypes.