sites, with the exception of genes such as the Hox loci at which they appear to act synergistically to enable the placement of the H3K27Me3 mark (11). This is in marked contrast to Drosophila, where BAF opposes Polycomb at the Hox genes (8). As yet, it is unclear whether humans follow the strategy observed in Drosophila or mice. Hence, in MRTs, the loss of BAF47 results in altered balance of the activity of BAF and Polycomb complexes, skewing toward Polycomb placement of repressive marks (Fig. 5).
