H3 acetylation triggers SWR1 recruitment to promote H2A.Z incorporation into chromatin and stimulate gene expression

Following DNA replication, the canonical H2A in eukaryotes is frequently replaced by histone variants, such as the conserved H2A.Z. Chromatin remodelers like the SWI/SNF-Related 1 (SWR1) complex facilitate this process, substituting the H2A histone with H2A.Z in an ATP-dependent manner. However, the precise mechanisms that recruit SWR1 to specific loci remain elusive. In this study, we investigate the role of H3 acetylation in mediating H2A.Z incorporation into chromatin to promote gene expression. Our results show that artificially induced hyperacetylation is associated with higher levels of H2A.Z and a decrease in H2A.W (HTA6 and HTA7). This phenomenon is also observed in genetic backgrounds that are defective in the histone deacetylases HISTONE DEACETYLASE 6 (HDA6) and HISTONE DEACETYLASE 9 (HDA9). Moreover, H2A.Z is required for the phenotypes observed in hda6-1 and hda9-1.