Figure 2.

Misexpression of Fezf2 in striatal MSNs or of Ptf1a in cortical pyramidal cells cell-autonomously promotes subtype-specific features. Misexpression studies of Fezf2 in the striatum and Ptf1a in the cortex, regions of the CNS where these transcription factors are not endogenously expressed, demonstrate their sufficiency to cell-autonomously promote features of a CFuPN or inhibitory peptidergic interneuron, respectively. Column 1 illustrates how misexpression of Fezf2 (+Fezf2) induces MSN identity to resemble that of CFuPNs. From top to bottom, this involves alterations in the MSN molecular profile, a change in cellular morphology from a stellate to a pyramidal morphology, the induction of axonal targeting toward subcortical targets, such as the spinal cord, and a shift toward a glutamatergic neurotransmitter status [34]. Column 2 illustrates how misexpression of Ptf1a (+Ptf1a) induces pyramidal cell identity to resemble that of inhibitory peptidergic interneurons. From top to bottom, this involves alterations in the pyramidal cell molecular profile, a change in cellular morphology from a pyramidal to a more radial, branched morphology, adoption of a tangential migration pattern and the induction of a primarily nociceptinergic neurotransmitter status [15,19]. Plus sign ‘+’ indicates an excitatory neurotransmitter status, minus sign ‘−’ indicates an inhibitory neurotransmitter status. glu, glutamate; noc, nociceptin.