Until several years ago, the mechanism of action of ATP-dependent chromatin remodeling complexes was thought to be fairly simple (25–28). They appeared to be recruited to DNA by sequence-specific transcription factors or general factors, and they subsequently attacked nucleosomes to facilitate the binding of proteins to DNA (29). Nucleosomes were thought to be the primary target of the complexes. Using in vitro transcription on nucleosomal templates, the complexes could phase or position nucleosomes, exchange nucleosomes, induce nucleosome mobility, evict nucleosomes, or relax torsional stress possibly by their direct actions on nucleosomes (28). However, doubts surrounding these mechanisms began to arise when it was discovered that the deletion of subunits of the mammalian complexes that gave the strongest phenotypes in mice were not required for in vitro chromatin remodeling (30, 31). Initially, this was thought to be due to a role for these subunits in specific targeting to regions of the genome. However, this explanation now seems unlikely because mutations in the subunits involved had phenotypes nearly identical to rapid conditional deletion of the Brg and/or Brm ATPase (32–35), indicating that
