Abstract

In mammals, combinatorial assembly of alternative families of subunits confers functional specificity to ATP-dependent SWI/SNF-like BAF chromatin remodeling complexes by creating distinct polymorphic surfaces for interaction with regulatory elements and DNA-binding factors. Increasing evidence indicates that specialized assemblies of BAF complexes regulate cell fate decisions throughout development, but little is known on the role of BAF complexes in normal and leukemic hemopoiesis. Using quantitative proteomics and molecular genetics approaches, we show that the transition from the quiescent to proliferative state of hemopoietic stem cells (HSCs) is accompanied by an exchange of alternative ATPases within hemopoietic-specific BAF complexes.

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