PBAF's genomic binding dynamics are regulated via bromodomain-acetyl-lysine interactions and select chromatin states.

Rapid changes in chromatin structure via the action of ATP-dependent chromatin-remodeling complexes are thought to dynamically regulate transcriptional bursting. Chromatin-remodeling complexes are targeted to genomic loci by histone post-translational modifications (PTMs) including acetylation. Despite extensive in vitro studies, much is still unknown about how chromatin-remodeling complexes rapidly bind genomic targets and function in vivo. We sought to understand how the PBAF chromatin-remodeling complex interacts with different chromatin states using live-cell single particle tracking of the BAF180 subunit. Dual color tracking of PBAF with either H3.3 or HP1α revealed that PBAF binds chromatin within actively transcribed regions for shorter time periods relative to heterochromatin. We also found that deletion of BAF180's six bromodomains reduced both the association and dissociation of PBAF with chromatin. Finally, elevation of histone acetylation levels increased the frequency of PBAF revisiting to genomic foci. Together, these results suggest that acetyl-lysine dependent clustered binding of PBAF to select genomic loci may facilitate rapid chromatin-remodeling in actively transcribed regions. Overall our work also indicates that the dynamics of chromatin state alterations proceed at fast timescales to potentially regulate transcriptional bursting.