ArticleLife science alliance2023
Methylation of lysine 36 on histone H3 is required to control transposon activities in somatic cells.
Article in Life science alliance, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Viral mimicry escape as a necessary feature of malignant transformation.Nature reviews. Cancer · 2026Review
- On the potential origin of the zygote-like cancer stem cell with a focus on fusion for cell rescue.Frontiers in cell and developmental biology · 2026Article
- Genomic context-dependent histone H3K36 methylation by three Drosophila methyltransferases and implications for dedicated chromatin readers.Nucleic acids research · 2025Article
- Transposons disrupt genomic stability and trigger cancers.Frontiers in cellular and infection microbiology · 2025Review
- Genomic context-dependent histone H3K36 methylation by three Drosophila methyltransferases and implications for dedicated chromatin readers.Nucleic acids research · 2024Article
- Recent reactivation of a pathogenicity-associated transposable element is associated with major chromosomal rearrangements in a fungal wheat pathogen.Nucleic acids research · 2024Article
- Generation of LexA enhancer-trap lines in Drosophila by an international scholastic network.G3 (Bethesda, Md.) · 2023Article
- Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transposable elements constitute a substantial portion of most eukaryotic genomes and their activity can lead to developmental and neuronal defects. In the germline, transposon activity is antagonized by the PIWI-interacting RNA pathway tasked with repression of transposon transcription and degrading transcripts that have already been produced. However, most of the genes required for transposon control are not expressed outside the germline, prompting the question: what causes deleterious transposons activity in the soma and how is it managed? Here, we show that disruptions of the Histone 3 lysine 36 methylation machinery led to increased transposon transcription in
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Registered trials
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