Bcl11b deletion also affects the maturation of vomeronasal sensory neurons (VSNs) which detect pheromones and project to the olfactory bulb (OB) (Dulac and Axel, 1995; Herrada and Dulac, 1997; Matsunami and Buck, 1997; Ryba and Tirindelli, 1997). In Bcl11b−/− mice, VSN precursors are produced normally and terminal differentiation is induced, but the immature VSNs display increased apoptosis, reduced axonal outgrowth and mistargeting to incorrect regions in the OB, leading to abnormal layer structure in the anterior olfactory bulb (AOB) (Enomoto et al., 2011). Transcriptionally, Bcl11b is necessary for activating the vomeronasal receptor genes V1r and V2r, as well as Big2/Contactin4, an axonal guidance molecule in the olfactory system. Bcl11b also has a role in finer subtype specification of VSNs, regulating the fate decision between basal and apical VSNs.
