Mutually exclusive binding of RNA Pol II and PRC2 explains the paradox in the antagonistic activities of NuRD and SWI/SNF at gene promoters. (A) Genome browser view for four representative genes (Cdk1, Ercc6l, Fam107b, and Ets1) that are bound by both CHD4 and BRG1 at their promoters. DNA accessibility of all four gene promoters is increased following Chd4 KD (light green) and is decreased following Brg1 KD. Also shown are gene expression fold changes following Chd4 or Brg1 KD (bottom), the orientation of which are opposite for high/average Pol II–bound genes and low Pol II–bound/bivalent genes. (B) A model to explain the differential activity of NuRD and SWI/SNF at Pol II–bound and PRC2-bound genes. (C) Changes in H3K27me3 modification at lowly expressed and bivalent gene promoters (PRC2-bound) following loss of BRG1 activity (left) and KO of Mbd3 (right). (D) Genome browser view for Fam107b (lowly expressed gene) where the loss in BRG1 activity leads to an increase in H3K27me3 modification. The opposite is observed following KO of Mbd3.
