Within a few years, similar complexes were discovered in Drosophila from genetic screens designed to detect genes opposing Polycomb-mediated repression of homeotic genes (8, 9). Notably, the ATPase subunit, of the complex in flies, Brm, was found to be homologous to SWI2 or SNF2. Significantly, revertants to mutations in Brm have never been found in histone genes, as is the case in yeast. Thus, it appeared that for the Drosophila SWI/SNF or BAP (Brm-associated protein) (10) complex, the primary targets were not histones, but rather opposing repressive complexes known as Polycomb complexes; however, because of the large number of histone genes, a dominant mutation in a histone may appear genetically invisible. Evidence indicating that Polycomb complexes are an important primary target of mammalian SWI/SNF or BAF complexes has emerged in more recent years from the observation that mutation of the ATPase Brg1 (Smarca4) of BAF complexes leads to H3K27Me3 accumulation and repression of many genes in embryonic stem (ES) cells (11). Additional evidence that BAF opposes Polycomb has come from studies of human malignancy, as will be discussed below (see
