The AtMYB44 promoter is accessible to signals that induce different chromatin modifications for gene transcription.

AtMYB44 transcripts accumulate non-specifically under diverse stress conditions and with various phytohormone treatments in Arabidopsis thaliana. We investigated the chromatin modifications caused by various signals to uncover the induction mechanism of AtMYB44 transcription. Bisulfite sequencing confirmed a previous database illustrating that the AtMYB44 promoter and gene-body regions are completely DNA methylation-free. Chromatin immunoprecipitation (ChIP) assays revealed that the nucleosome density is remarkably low at the AtMYB44 promoter region. Thus, the promoter region appears to be highly accessible for various trans-acting factors. ChIP assays revealed that osmotic stress (mannitol treatment) lowered the nucleosome density at the gene-body regions, while abscisic acid (ABA) or jasmonic acid (JA) treatment did so at the proximal transcription start site (TSS) region. In response to mannitol treatment, histone H3 lysine 4 trimethylation (H3K4me3) and H3 acetylation (H3ac) levels within the promoter, TSS, and gene-body regions of AtMYB44 were significantly increased. However, occupancy of histone variant H2A.Z was not affected by the mannitol treatment. We previously reported that salt stress triggered a significant decrease in H2A.Z occupation without affecting the H3K4me3 and H3ac levels. In combination, our data suggest that each signal transduced to the highly accessible promoter induces a different chromatin modification for AtMYB44 transcription.