The function of BAF53B in dendritic morphogenesis cannot be replaced by BAF53A, demonstrating the functional specialization of BAF complexes of different compositions. Genes encoding several subunits of BAF complexes were also found in an RNAi screen for factors involved in dendritic morphogenesis in D. melanogaster37, indicating that there is a conserved chromatin-regulatory program of dendritic morphogenesis. Interestingly, the downregulation of BAF53A during neuronal differentiation in mice is mediated by two microRNAs (miRNAs): miR-9* and miR-124 (ref. 38). These miRNAs are targeted by REST, a transcriptional repressor that is selectively downregulated in post-mitotic neurons. Mutating the miRNA-binding sites in the 3′-untranslated region of BAF53A gene leads to prolonged expression of BAF53A and reduced amounts of BAF53B in post-mitotic neurons. In accordance with the neuron-specific function of BAF53B, the persistent expression of BAF53A in neurons causes defects in activity-dependent dendritic outgrowth, illustrating the biological significance of subunit switching in BAF complexes during neural development. These studies suggest that the tissue-specific BAF complexes that arise from combinatorial assembly might allow matching between chromatin-remodelling complexes and ambient transcription factors, such as CREST in the case of post-mitotic neurons.
