After embryonic development, neurogenesis ceases in most regions of the CNS. The subependymal zone (SEZ) in the lateral walls of the lateral ventricles is one of the two neurogenic niches in the adult brain, and supplies new neurons to the olfactory bulb (OB) (Luskin, 1993; Lois and Alvarez-Buylla, 1994) as well as glia to the cortex and corpus callosum (Menn et al., 2006) throughout life. Adult NSCs have similar properties to embryonic NSCs and are thought to arise from the latter (Ahlenius et al., 2009). The precise composition of BAF complexes in adult NSCs is unknown, but Brg1 has been shown to suppress non-neuronal fates in this context while, intriguingly, not affecting self-renewal. The interaction between Pax6 and the Brg1-containing BAF complex is essential for specifying the neurogenic fate of adult NSCs in the SEZ (Ninkovic et al., 2013): ablation 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,
