Smarca4 ATPase mutations disrupt direct eviction of PRC1 from chromatin

Gerald Crabtree, Keji Zhao and colleagues report that recurrent disease-associated mutations in SMARCA4 result in increased PRC1 deposition and activity. Using an in cellula assay, they find that the BAF (mSWI/SNF) complex directly evicts PRC from chromatin via an ATP-dependent mechanism and that this occurs within minutes of BAF occupancy.