ArticleNucleic acids research2022
OCT4 activates a Suv39h1-repressive antisense lncRNA to couple histone H3 Lysine 9 methylation to pluripotency.
Article in Nucleic acids research, 2022. 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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8 citing papers in PubMed, 15 citations in OpenAlex.
- Mechanisms coordinating exit from the stem cell state in mammals.Genes & development · 2026Review
- Brain transcriptome analysis reveals novel long non-coding RNAs in Dryophytes arenicolor (Canyon Treefrog).G3 (Bethesda, Md.) · 2026Article
- Antisense transcription can induce expression memory via stable promoter repression.Genome biology · 2025Article
- Molecular and epistatic interactions between pioneer transcription factors shape nucleosome dynamics and cell differentiation.Nature communications · 2025Article
- H3K9 post-translational modifications regulate epiblast/primitive endoderm specification in rabbit blastocysts.Epigenetics & chromatin · 2025Article
- Crosstalk between Noncoding RNAs and the Epigenetics Machinery in Pediatric Tumors and Their Microenvironment.Cancers · 2023Review
- H3K9 tri-methylation at Nanog times differentiation commitment and enables the acquisition of primitive endoderm fate.Development (Cambridge, England) · 2022Article
- Methylation hallmarks on the histone tail as a linker of osmotic stress and gene transcription.Frontiers in plant science · 2022Review
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Authors and funding
15 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone H3 Lysine 9 (H3K9) methylation, a characteristic mark of heterochromatin, is progressively implemented during development to contribute to cell fate restriction as differentiation proceeds. Accordingly, in undifferentiated and pluripotent mouse Embryonic Stem (ES) cells the global levels of H3K9 methylation are rather low and increase only upon differentiation. How global H3K9 methylation levels are coupled with the loss of pluripotency remains largely unknown. Here, we identify SUV39H1, a major H3K9 di- and tri-methylase, as an indirect target of the pluripotency network of Transcription Factors (TFs). We find that pluripotency TFs, principally OCT4, activate the expression of Suv39h1as, an antisense long non-coding RNA to Suv39h1. In turn, Suv39h1as downregulates Suv39h1 transcription in cis via a mechanism involving the modulation of the chromatin status of the locus. The targeted deletion of the Suv39h1as promoter region triggers increased SUV39H1 expression and H3K9me2 and H3K9me3 levels, affecting all heterochromatic regions, particularly peri-centromeric major satellites and retrotransposons. This increase in heterochromatinization efficiency leads to accelerated and more efficient commitment into differentiation. We report, therefore, a simple genetic circuitry coupling the genetic control of pluripotency with the global efficiency of H3K9 methylation associated with a major cell fate restriction, the irreversible loss of pluripotency.
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