H3 Acetylation promotes H2A.Z incorporation into chromatin through SWR1 recruitment to stimulate expression.

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: ChIP-seq of H2A.Z?H3K9K14Ac?H3K18Ac in Columbia-0(WT) and hda6-1 mutant background; ChIP-seq of H2A.Z?H3K9K14Ac?H3K27Ac in Columbia-0(WT) and hda9-1 mutant.ChIP-seq of H2A?H2A.X in Columbia-0(WT) background;ChIP-seq of HTA67 in Columbia-0(WT) and h2az-5 mutant background.ChIP-seq of H3?H3K9K14Ac?H3K27Ac?H2A.Z?HTA67?HTA12 in Columbia-0(WT) and Columbia after TSA treatment. Plants used for ChIP-Seq and TSA treatments were grown in MS media supplemented with 1% sucrose under long-day photoperiod and ~21°C. In all cases, seeds were stratified for 4 days at 4°C, and seedlings were harvested 12 days after germination.