Functional nBAF complexes have an essential role in dendritic morphogenesis, a process which is critical for the proper integration of postmitotic neurons into their appropriate circuitry (Jan and Jan, 2003; Whitford et al., 2002). This is conserved in flies, where perturbation of BAP55, BRM, BAF60 or SNR1 (fly homologs of BAF53a/b, BRM, BAF60c and BAF47) results in PNS dendritic morphogenesis defects (Parrish et al., 2006); in addition, the loss of BAP55 produces a highly specific, fully penetrant retargeting phenotype in Drosophila olfactory projection neurons and can be rescued by expressing the human BAF53A or BAF53B (Tea and Luo, 2011). Deletion of ham-3 (homolog of BAF60) in C. elegans, on the other hand, disrupts axon pathfinding in a specific subset of serotonergic neurons (Weinberg et al., 2013).
