a specific thinning of the upper cortical layers due to premature asymmetrical cell division of the progenitors (Estivill-Torrus et al., 2002). BAF has been shown to interact with Pax6 to regulate the decision between direct and indirect neurogenesis (Tuoc et al., 2013). Specifically, BAF170-containing npBAF complex restricts indirect neurogenesis during the early phase by recruiting the transcriptional repressor REST to Pax6 targets (Tuoc et al., 2013; Battaglioli et al., 2002). Notably, the amino acid sequences of BAF170 and BAF155 diverge the most in the C-terminal region, and it is the C-terminus of BAF170 that is required for its interaction with REST in vitro. The loss of BAF170 in Emx1+ cortical progenitors has the opposite effect from Pax6 deletion and causes an abnormal expansion of IPs and a bias toward upper-layer identities, while BAF170 overexpression causes a phenotype similar to the Pax6-null with a depletion of upper-layer neurons (Tuoc et al., 2013). Thus, specific assemblies of npBAF determine the size as well as composition of the cortex.
