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<p>Heterochromatin formation is pivotal in many eukaryotes with repetitive sequences, such as transposable elements (TEs). However, in plants, where the known de novo DNA methylation mechanism (RdDM) targets euchromatin, how heterochromatin is formed in a region-specific manner remains unclear. We previously reported an RdDM-independent de novo establishment of H3K9me and non-CpG methylation, both of which localize in heterochromatin. Here we show that the mutually exclusive histone H2A variants, H2A.W and H2A.Z, function as guides to initiate heterochromatin formation; H2A.W and H2A.Z promotes and inhibits heterochromatin establishment, respectively, especially in chromosomal arm regions with dispersed TEs. In contrast, pericentromeric TEs demonstrate autonomous heterochromatin formation, less dependently on these H2A variants. Furthermore, H2A.Z protects protein-coding genes from ectopic heterochromatin formation, possibly by preventing its spreading. We propose that the genome indexing mechanism driven by H2A variants, as well as the autonomous formation of pericentromeric heterochromatin, shapes proper epigenomic patterns in Arabidopsis.</p>

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Antagonistic histone H2A variants and autonomous heterochromatin formation shape epigenomic patterns in Arabidopsis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月30日

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  • Shoko Oda,
  • Sayaka Tominaga,
  • Shumpei Takeuchi,
  • Akihisa Osakabe,
  • Akira Kawabe,
  • Frédéric Berger,
  • Tetsuji Kakutani,
  • Taiko Kim To

摘要

Heterochromatin formation is pivotal in many eukaryotes with repetitive sequences, such as transposable elements (TEs). However, in plants, where the known de novo DNA methylation mechanism (RdDM) targets euchromatin, how heterochromatin is formed in a region-specific manner remains unclear. We previously reported an RdDM-independent de novo establishment of H3K9me and non-CpG methylation, both of which localize in heterochromatin. Here we show that the mutually exclusive histone H2A variants, H2A.W and H2A.Z, function as guides to initiate heterochromatin formation; H2A.W and H2A.Z promotes and inhibits heterochromatin establishment, respectively, especially in chromosomal arm regions with dispersed TEs. In contrast, pericentromeric TEs demonstrate autonomous heterochromatin formation, less dependently on these H2A variants. Furthermore, H2A.Z protects protein-coding genes from ectopic heterochromatin formation, possibly by preventing its spreading. We propose that the genome indexing mechanism driven by H2A variants, as well as the autonomous formation of pericentromeric heterochromatin, shapes proper epigenomic patterns in Arabidopsis.