While rodent studies have informed much of what we know about human neural development, the human brain has undergone tremendous evolution particularly in the neocortex, with a concomitant increase in the complexity of precursor-progeny relationships. For instance, a small subset of human GABAergic interneurons originates from precursors whose final mitotic division takes place in the dorsal telencephalon (Letinic et al., 2002). An even more striking difference in the human is a massive expansion of a novel population of RGs, termed outer RGs (oRGs), which lack the apical process of ventricular RGs (vRGs) and reside in the outser SVZ (oSVZ) (Hansen et al., 2010; Fietz et al., 2010; Wang et al., 2011). Although oRGs do not undergo the highly stereotyped interkinetic nuclear movement (INM) of vRGs during mitosis (Noctor et al., 2004), instead exhibiting mitotic somal translocation (MST) (LaMonica et al., 2013), the two RG populations display similar cycling kinetics. Understanding how BAF contributes to the regulation of this novel population of progenitors may shed light on the emergence of human-specific cognitive traits and their disruption in disease states.
