Similar to the role of esBAF in ES cells, components of the nBAF complex have a critical role in the self-renewal of neural progenitors. Mice heterozygous for Brg1 or BAF155 have defects in neural tube closure, indicative of insufficient cell numbers (Bultman et al., 2000; Kim et al., 2001). The rate-limiting role of BAF in progenitor division is evolutionarily conserved: in C. elegans, the asymmetric division of NSCs requires psa-1 and psa-4 (homologs of BRG1 and BAF155, respectively) (Sawa et al., 2000). Deleting Brg1 specifically in Nestin+ murine NSCs causes reduced proliferation and subsequent depletion of the neural progenitor pool; these mice die perinatally and exhibit thinning of the cortex and midbrain, as well as near-complete absence of the cerebellum (Matsumoto et al., 2006; Lessard et al., 2007; Zhan et al., 2011). Interestingly, even though the total number of GFAP+ astrocytes is reduced in the Nestin::Brg1−/− animals, the astrocytes themselves are not impaired in their ability to divide, indicating that the effect on proliferation is specific to the multipotent progenitors. At the transcriptional level, Brg1-containing npBAF complexes activate Notch signaling
