of either Pax6 or Brg1 diverts adult NSCs from the neuronal lineage to the ependymal or glial lineages. Gene expression profiling of Brg1-deleted SEZ and OB shows misregulation of genes involved in cell cycle, neurogenesis, axonogenesis and synaptic transmission. Surprisingly, Brm is unable to compensate for Brg1 in adult NSCs despite being expressed at high levels. The interaction of BAF with Pax6 seems functionally specific: forced neurogenesis by Pax6 expression in SEZ-derived neurospheres requires a catalytically active form of Brg1, whereas overexpression of another neurogenic transcription factor, Ngn2, efficiently generates neurons in the absence of Brg1 (Ninkovic et al., 2013). Therefore, the interaction between Pax6 and BAF, which also regulates embryonic neural progenitor division (Tuoc et al., 2013), may have been repurposed for adult neurogenesis in the SEZ.
