Recent studies have indicated that BAF complexes help TopoII untangle DNA during replication, perhaps providing an explanation for BAF’s tumor-suppressive functions (Fig. 6). At each cell division, hundreds or even thousands of catenes must be relieved by passing one strand of DNA through another (115). This risky task is carried out by TopoIIα and TopoIIβ by first cleaving one strand with a 4–base pair overlap and then forming a covalent bond between the enzyme and DNA. Because the enzyme is a dimer, it can hold a first strand in place while creating a channel for the passage of the second strand. Afterward, the two ends are ligated together by TopoII, relieving the tangle and allowing cell division to proceed (116, 117). Deletion or shRNA depletion of the oncogenic BAF subunits leads to the formation of anaphase bridges, indicating a failure to untangle DNA at anaphase, whereas deletion of non-oncogenic subunits did not have this effect (97). The deletion of oncogenic BAF subunits surprisingly leads to arrest at G2/M with high levels of histone H3 S-10 phosphorylation, an indicator of incomplete
