Smarcb1 is indispensable for the nervous system development and its loss results in a deregulation of esBAF binding [ChIP-seq]

Using ChIP-seq technology, we aimed to provide insight into the consequences of the knockdown of Smarcb1, an essential esBAF subunit, for the binding of the esBAF complex (Smarca4), the PRC2 complex (Ezh2) as well as for histone marks H3K27me3, H3K27ac and H3K4me3. We show that Smarcb1 knockdown results in the change of BAF complex binding in both directions: decreased binding (potentially by loss of function) as well as increased binding (potentially by retargeting). Furthermore, we see that binding changes especially occur in regions important for basic cellular functions (adhesion, cell organization, metabolism) as well as regions crucial for development (especially nervous system development). In addition, we depicted binding changes in enhancer regions in which a decrease of BAF binding was much more prominent than in gene regions. Overall design: Genome-wide binding of Smarca4, Ezh2, H3K27me3, H3K27ac and H3K4me3 in Smarcb1 wildtype and Smarcb1 knockdown mESC