In vertebrates, ATP-dependent chromatin remodeling is mediated by BAF complexes, which are the functional equivalents of the SWI/SNF complexes in yeast. The human BAF complex consists of 15 subunits, where one of both homologue ATPase core subunits, SMARCA4 or SMARCA2, is always present [Ronan et al., 2013]. Additional components vary with developmental stage and tissue, with theoretically several hundred possible configurations. The exact subunit composition of the complex determines the final functional characteristics and tissue specificity. With regard to neuronal development, a switch of three subunits in the complex composition predisposes the neuronal progenitor cells to a post-mitotic state and initiates activity-dependent dendritic outgrowth and axonal development. This transition occurs in all neurons, and illustrates the fundamental role of BAF complexes in development [Lessard et al., 2007]. Defects hampering the global function of the complex can result in multiple defects in an organism [Ho and Crabtree, 2010]. Illustrative for these global effects of deregulating BAF-mediated chromatin remodeling is that mutations in six components of the neuronal BAF (nBAF) complex (SMARCB1, SMARCA4, SMARCA2, SMARCE1, ARID1A, and ARID1B) have been reported to
