This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility: Histone variants help establish DNA methylation at transposons (jumping genes) while preventing this epigenetic modification from spreading to essential genes in plants, a study from the Institute of Science Tokyo reveals. By revealing how these chromosome-associated proteins guide the formation of precise epigenomic patterns, the findings provide new insights into the selective silencing of transposons, laying the groundwork for future epigenome-editing technologies for crop improvement and disease research.
Plants and animals have multiple transposons, or "jumping genes," in their genomes. These mobile DNA elements can move to new locations within the genome. Although transposons have contributed to genome evolution, their movement can disrupt genes and compromise genome stability, leading to diseases such as cancer.
To prevent this, organisms often rely on epigenetic mechanisms (cellular processes such as DNA methylation that control gene expression without changing the underlying DNA sequence) to keep transposons inactive. But as transposons and essential genes coexist within the same genome, an important question arises: How do cells selectively target transposons without accidentally silencing essential genes? To address this question, a research team led by Associate Professor Taiko Kim To and Dr.
Shoda Oda from the Department of Life Science and Technology, School of Life Science and Technology, Institute of Science Tokyo (Science Tokyo), Japan, investigated the role of histone variants (slightly different forms of the histone proteins around which DNA is wrapped) in establishing DNA methylation. Their findings are published in Nature Communications. Using genetically engineered mutants of the model plant Arabidopsis thaliana lacking specific histone variants, the researchers restored DNA methylation through selective regulation and tracked how epigenetic patterns were reestablished across the genome under different histone variant compositions.
The experiments revealed that the histone variant H2A.W promotes DNA methylation at transposons, facilitating their inactivation. In contrast, H2A.Z suppresses DNA methylation and is enriched in gene regions, where it protects important genes from being mistakenly silenced. "We observed that these opposing functions were particularly evident in gene-rich regions of the genome, where accurate epigenetic regulation is especially critical," To said.
The findings demonstrate that histone variants act as molecular guides that determine where DNA methylation should be established by enabling plants to selectively inactivate transposons while preserving normal gene activity. The study also reveals that the genomic environment influences how epigenetic patterns are restored. In chromosome arms rich in essential genes, transposons are dispersed among the genes.
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