During pre- and postnatal hippocampal development, Bcl11b expression is again restricted to postmitotic granule neurons and excluded from the dividing progenitors in the subgranular zone (SGZ) of the dentate gyrus (Simon et al., 2012). In the Bcl11b-null brain, newborn neurons have reduced calbindin 1 (Calb1) expression, are no longer confined to the innermost compartment of the granule cell layer (GCL) and have shorter dendrites than wild-type, reminiscent of the dendritic outgrowth phenotype seen in BAF53b−/− hippocampal neurons in vitro (Wu et al., 2007). Intriguingly, there is a severe reduction in the size and cell number of the dentate gyrus in the absence of Bcl11b due to a decrease in BrdU+ progenitors without increased apoptosis (Simon et al., 2012); given the exclusion of Bcl11b from the progenitors in the SGZ in wild-type animals, this suggests indirect mechanisms are at work. It will be of interest to examine whether Bcl11b-containing BAF complexes cooperate with subtype-specific transcription factors to target distinct chromatin loci for activation or repression in each neuronal type.
