ArticleNucleic acids research2025
DNA methylation dictates histone modifications in developing male germ cells in the mouse.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Transposable element regulation in mammalian germ cells and other contexts: multilayered repression, fertility, and regulated activation.Epigenomics · 2026Review
- piRNA: Molecular Mechanisms from Germline Silencing to Somatic Regulation and Roles in Disease.International journal of molecular sciences · 2026Review
- Understanding Cancer Health Disparities.Cancers · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
In the male germline of mammals, retrotransposon expression is restricted by DNA methylation, trimethylation of histone H3 at lysine 9 (H3K9me3), and PIWI-interacting small RNAs (piRNAs). To elucidate their relative importance in regulating retrotransposons during germ cell development and the relationships between these mechanisms, we performed mRNA sequencing, DNA methylation, and histone methylation analyses using mouse spermatogonia from Dnmt3l and Pld6 mutants deficient in de novo DNA methylation and piRNA production, respectively. The results revealed that loss of DNA methylation resulted in decreased H3K9me3 in young L1 subfamilies and increased H3K4me3 in many retrotransposons, suggesting a pivotal role of DNA methylation in maintaining epigenomic integrity in spermatogonia and later stages of spermatogenesis. The transcriptional up-regulation of retrotransposons by a loss of DNA methylation was more evident during meiosis (spermatocytes) than before meiosis (spermatogonia). These results are aligned with a global reduction of H3K9me3 at retrotransposons in spermatocytes. The piRNA system also regulated H3K9me3 and H3K4me3 at retrotransposons in spermatogonia, probably through the regulation of DNA methylation, since the loss of DNA methylation resulted in decreased H3K9me3 and increased H3K4me3 at the same retrotransposon loci even in the presence of piRNAs.
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Registered trials
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