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<p>5-methylcytosine (5mC) DNA methylation is an ancient epigenetic mechanism. Methyl-CpG-binding domain protein 2 or 3 (MBD2/3) is a component of the Nucleosome Remodeling and Deacetylase (NuRD) complex, essential for gene regulation in mammals. The MBD2/3 ortholog is surprisingly preserved even in 5mC-free invertebrates, such as nematodes and flies. We found that <i>Caenorhabditis elegans</i> MBD-2 (<i>Cel</i>-MBD-2), despite without the MBD domain, is a conserved component of the NuRD complex. <i>Cel</i>-MBD-2 null mutation or deletion of its NuRD-interacting coiled-coil domain causes morphological defects and infertility. While a minority of <i>Cel</i>-MBD-2 colocalizes with NuRD at active chromatin, the majority of <i>Cel</i>-MBD-2 localizes to repressive chromatin environments enriched with H3K27me3 and H3K9me2/3, not overlapping with NuRD. The mechanism by which <i>Cel-</i>MBD-2 localizes to the repressive chromatin is still unknown, but is independent of NuRD or MBD-5mC interaction. The potential compensation of DNA methylation by histone modifications highlights the adaptability of epigenetic regulation during evolution.</p>

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Dual genomic localizations and gene regulatory functions of MBD-2 with and without NuRD in Caenorhabditis elegans which lacks DNA methylation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月20日

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  • Hok Ning Tsui,
  • Charmaine Yan Yu Wong,
  • Chaogu Zheng,
  • Karen Wing Yee Yuen

摘要

5-methylcytosine (5mC) DNA methylation is an ancient epigenetic mechanism. Methyl-CpG-binding domain protein 2 or 3 (MBD2/3) is a component of the Nucleosome Remodeling and Deacetylase (NuRD) complex, essential for gene regulation in mammals. The MBD2/3 ortholog is surprisingly preserved even in 5mC-free invertebrates, such as nematodes and flies. We found that Caenorhabditis elegans MBD-2 (Cel-MBD-2), despite without the MBD domain, is a conserved component of the NuRD complex. Cel-MBD-2 null mutation or deletion of its NuRD-interacting coiled-coil domain causes morphological defects and infertility. While a minority of Cel-MBD-2 colocalizes with NuRD at active chromatin, the majority of Cel-MBD-2 localizes to repressive chromatin environments enriched with H3K27me3 and H3K9me2/3, not overlapping with NuRD. The mechanism by which Cel-MBD-2 localizes to the repressive chromatin is still unknown, but is independent of NuRD or MBD-5mC interaction. The potential compensation of DNA methylation by histone modifications highlights the adaptability of epigenetic regulation during evolution.