The precise biophysical mechanism of ATP-dependent chromatin remodelers is not well understood; however, loosening heterochromatic loci across the genome appears to be a critical function of BAF. This is achieved at least in part by antagonizing the repressive Polycomb complexes and facilitating the removal of H3K27me3 – a conserved regulatory interaction which co-emerged with multicellularity. The accessibility thus created by BAF allows other nuclear factors that interact with BAF, such as STAT3, Pax6 and REST, to bind their genomic targets and regulate downstream genes in a context-dependent manner. The composite surfaces created by the assembly of cell type-specific subunit combinations may dictate the versatility of BAF interactions. Of note, BAF also cooperates with lineage-specifying transcription factors during the differentiation of oligodendrocytes and Schwann cells (Limpert et al., 2013; Marathe et al., 2013), which are the glial cells responsible for myelinating axons in the CNS and PNS, respectively.
