Abiotic stresses, including drought, salinity, temperature fluctuations, and nutrient deficiencies, challenge plant growth and productivity, requiring adaptive mechanisms for survival. Histone modifications, especially histone methylation, participate in gene expression regulation in response to these stresses. Notably, bivalent H3K4me3–H3K27me3 modifications play a central role in fine-tuning stress-responsive genes, allowing plants to adapt to environmental changes. Recent studies have highlighted the dynamic switching of these bivalent chromatin marks at specific loci during stress, facilitating plant acclimatization to adverse environments. This review focuses on the four major histone H3 methylation modifications—H3K4, H3K9, H3K27, and H3K36—examining the roles of the associated methyltransferases and demethylases in mediating histone methylation dynamics. We synthesize recent findings on how these modifications regulate plant responses to various abiotic stresses, such as drought, salinity, heat, light stress, heavy metal exposure, and nutrient stress. By exploring these molecular mechanisms, we aim to deepen our understanding of how histone methylation shapes plant stress responses at both transcriptional and epigenetic levels. Furthermore, we also discuss the functional interaction of histone methylation with histone acetylation. These insights are critical for advancing breeding strategies aimed at improving plant tolerance to environmental stressors, ensuring food security, and supporting sustainable agricultural practices amid climate change.

Rice straw presents challenges as livestock feed due to its low digestibility and the presence of chemical residues. One potential solution is to focus on breeding brittle varieties that possess disease-resistance traits. In this study, AZ1803, a brittle mutant line isolated from the IR64 mutant pool, was chosen for gene identification and breeding. The AZ1803 mutant was crossed to the TNG67 variety to generate a mapping population and to the CS11 variety for fine mapping and breeding. The gene was mapped on chr. 10 between RM467 and RM171 SSR markers and was narrowed down to RM271 and RM5392 with 600 kb proximately interval. The AZ1803 and IR64 sequencing results revealed a substitution mutant in the Exon 9th of the OsCesA7 gene, resulting in an amino acid mutation at the end of the transmembrane domain 5th of the CESA7, responsible for cellulose synthesis for the secondary cell wall. The cellulose content of AZ1803 was reduced by 25% compared with the IR64. A new brittle and disease-resistant variety was bred by using developed markers in marker-assisted selection. In addition, bending tests and bacterial blight inoculation were applied. The bacterial lesion length of the bred variety is 64% lower than that of AZ1803. The rice straw of the new variety can be used for livestock feeding, which increases farmer income and reduces pesticide residues and air pollution from straw burning.

Polycomb repressive complex 2 (PRC2) is a conserved multi-protein complex that catalyzes histone H3 trimethylation at lysine 27 (H3K27me3), an epigenetic mark associated with transcriptional repression. However, the mechanistic link between PRC2-mediated H3K27me3 and light-regulated hypocotyl elongation during photomorphogenesis remains largely unexplored. In this study, we identify the MULTICOPY SUPPRESSOR OF IRA1 (MSI1), a core component of PRC2, as a negative regulator of hypocotyl elongation under light conditions in Arabidopsis thaliana. MSI1 physically interacts with ELONGATED HYPOCOTYL 5 (HY5), a basic leucine zipper (bZIP) transcription factor central to photomorphogenic signaling, in vitro and in vivo. Genetic and molecular analyses reveal that MSI1 is indispensable for HY5-mediated repression of hypocotyl growth, suggesting a cooperative function between chromatin-based silencing and transcriptional regulation. Chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq) showed that MSI1 and HY5 co-occupy numerous genomic loci. HY5 facilitates PRC2 complex recruitment to the target genes by interacting with MSI1, thereby promoting H3K27me3 deposition and repressing gene expression. Furthermore, transcriptomic profiling reveals that MSI1 and HY5 jointly suppress a subset of genes involved in auxin signaling, providing mechanistic insight into their role in photomorphogenesis. Together, our findings uncover an epigenetic mechanism by which HY5 recruits PRC2 through MSI1 to modulate light-responsive growth.