H2A.Z in drought stress

Response to abiotic stresses involves different regulatory mechanisms of gene expression. Chromatin states may contribute to the stress response, however, our understanding of their role in this process remains elusive. Here, by analysis of the arp6 mutant, which is impaired in deposition of the histone variant H2A.Z, and by H2A.Z profiling in abiotic stress conditions we investigated the impact of this histone variant on the expression of stress-related genes. We demonstrate that the arp6 mutant exhibits phenotypic defects in response to osmotic stresses, indicating a misregulation of corresponding genes. Indeed, RNA-sequencing revealed that among genes upregulated in arp6 the stress-responsive group is overrepresented. Genes upregulated in arp6 exhibit high levels of H2A.Z in gene bodies. Furthermore, we observed that H2A.Z distribution in genes induced and repressed in stress conditions significantly differs from that of constitutively active genes, and H2A.Z distribution does not change upon transcriptional activation or repression. However, occupancy of H2A.Z changes in parallel to gene transcriptional changes. In particular, we observed H2A.Z loss upon transcriptional activation and H2A.Z gain upon repression, which is consistent with a repressive role of H2A.Z in gene expression. In addition, our data indicate that H2A.Z at the first nucleosome downstream from transcription start site (+1) facilitates transcription initiation for constitutive and stress-repressed genes, but is less important for stress-induced genes. We propose that longer nucleosome depleted regions of stress-induced genes are responsible for binding additional transcription co-activators to overcome the +1 nucleosome barrier upon induction.