H3 Acetylation promotes H2A.Z incorporation into chromatin through SWR1 recruitment to stimulate expression [RNA-Seq]

Following DNA replication, canonical H2A in eukaryotes is frequently replaced by histone variants, such as the conserved H2A.Z. Chromatin remodelers like the 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 partially studied. In this study, we investigate the role of H3 acetylation in mediating the incorporation of H2A.Z into the 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 histone deacetylases HDA6 and HDA9 defective backgrounds. Moreover, H2A.Z is required for the phenotype observed in hda6-1 and hda9-1 Overall design: RNA-Seq of Columbia nrp1-1 nrp2-2 double mutant? hda6-1 mutant ?hda6-1 nrp1-1 nrp2-2 triple mutant ?hda9-1 mutant and hda9-1 nrp1-1 nrp2-2 triple mutant.RNA-Seq of Columbia and Columbia after TSA treatment. RNA-Seq data presented in this study were generated from three or five independent biological replicates: TSA-treated tissues were analyzed using five biological replicates, while mutant samples were evaluated with three biological replicates.