In addition, some of the subunits were found to be tissue-specific, such as those found only in BAF complexes of mature neurons (Fig. 2). For example, BAF53b (an actin-like molecule), BAF45b [a double plant homeodomain (PHD) finger protein], and CREST (SS18L1) (a Ca2+-responsive regulator) subunits were found only in postmitotic neurons (19, 20, 55, 56). These subunits appeared during evolution as a more complex brain with greater diversity of neurons came onto the evolutionary scene (Fig. 1). Forcing the assembly of this neuron-specific nBAF complex in human fibroblasts can convert them to neurons (31, 38), and knocking out the neuron-specific nBAF subunits leads to profound defects in critical postmitotic neuronal function such as dendritic outgrowth and synaptogenesis (49, 57). Following these reports, exome sequencing studies of human neurologic diseases revealed that individuals with language acquisition deficiencies with or without mental retardation (Coffin-Siris syndrome and Nicolaides-Baraitser syndrome) generally have mutations in one of several subunits of the BAF complex (43, 44). These discoveries have led to a search for tissue-specific and/or instructive roles for other chromatin remodeling and histone modification complexes. These studies and the finding that minor changes in subunit composition could result in malignancy (see below) put forward the
