In eukaryotes, histone lysine (K) methylation is important for regulating gene expression. K residues at the N-terminus of histone H3 or H4 can be monomethylated, dimethylated, or trimethylated, and the methylation of specific K residues, as well as the number of methyl groups added, can mark different chromatin states . Methylation of H3K4 and H3K36 is often associated with activation of gene transcription, while methylation of H3K9 and H3K27 is associated with repression of gene expression.
In animals, h3k4me2 and H3K4me3 are enriched at transcription start sites (TSS) and function as epigenetic marks regulating gene transcription, but their functions in plants have not been fully characterized.
We used chromatin immunoprecipitation sequencing to analyze genome-wide H3K4me1/ h3k4me2 /H3K4me3 changes in rice following deletion of the H3K4-specific methyltransferase SDG701. Knockdown of SDG701 resulted in a global decrease in h3k4me2/H3K4me3 levels throughout the rice genome. RNA-sequencing analysis revealed that many genes associated with different developmental processes were misregulated in SDG701 knockdown mutants. In rice, H3K4me3 and H3K36me3 were positively correlated with gene transcription; however, surprisingly, h3k4me2 levels were negatively correlated with gene transcription levels. Furthermore, among the genes whose expression was downregulated in SDG701, the level of H3K4me3 in the TSS region was significantly reduced in knockdown mutants. In contrast, up-regulated genes in the mutant were associated with significantly lower levels of H3K4me2 in the gene body region.
Comparison of the genome-wide distribution of h3k4me2 in eukaryotes showed that h3k4me2 levels did not correlate with gene transcription levels in yeast, but were positively and negatively correlated with gene expression in animals and plants, respectively. Our findings reveal h3k4me2 as a novel repressive marker in plants.
DNA damage can lead to cancer, impair development and accelerate aging. Transcription-blocking lesions and defects in transcription-coupled repair lead to developmental disorders and premature aging in humans. Following DNA repair, homeostatic processes need to be re-established to ensure development and maintain tissue function. Here, we report that depletion of the WRAD complex of the MLL/COMPASS H3K4 methyltransferase in C. elegans exacerbates developmental delay and accelerates senescence, while depletion of the H3K4 demethylases SPR-5 and AMX-1 reduces Promotes developmental growth and prolongs lifespan in UV-induced damage. DNA damage-induced h3k4me2 was shown to be involved in gene activation that regulates RNA transport, splicing, ribosome biogenesis, and proteostasis, and regulates the restoration of protein biosynthesis, thereby ensuring survival after genotoxic stress. Studies reveal a role for h3k4me2 in coordinating the restoration of protein biosynthesis and homeostasis required for developmental growth and longevity following DNA damage.