ArticleNature communications2026
Dual genomic localizations and gene regulatory functions of MBD-2 with and without NuRD in Caenorhabditis elegans which lacks DNA methylation.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
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.
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