ArticleEpigenetics & chromatin2016
Setdb1-mediated H3K9 methylation is enriched on the inactive X and plays a role in its epigenetic silencing.
Article in Epigenetics & chromatin, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 80 citations in OpenAlex.
- Multiomics integration uncovers metabolic control of H3K27ac in bovine inner cell masses†.Biology of reproduction · 2026Article
- Chromatin binding and N-terminal domains of DNMT3B1 confer specificity for developmentally regulated CpG island methylation.Genes & development · 2026Article
- SETDB1 and HUSH modulate Xist RNA levels during establishment of X chromosome inactivation.Nature communications · 2026Article
- Xist RNA dependent and independent mechanisms regulate dynamic X chromosome inactivation in B lymphocytes.Cell reports · 2026Article
- Establishment and Maintenance of Repressed Chromatin States on Dosage-Compensated Sex Chromosomes.Biomolecules · 2026Review
- The X Factor in Immunity: Sex Differences Shaped by the X Chromosome.Immunological reviews · 2026Review
- Impact of somatic XIST deletions on ongoing XIST expression and inactive X silencing and heterochromatin.Human molecular genetics · 2025Article
- Establishment of sex-specific liver transcriptomes and H3K9me3 profiles during sexual maturity: the impact of maternal obesity.Biology of sex differences · 2025Article
- Xist condensates: perspectives for therapeutic intervention.Genome biology · 2025Review
- Retrospective and multifactorial single-cell profiling reveals sequential chromatin reorganization during X inactivation.Nature cell biology · 2025Article
- Chromatin modifiers in neurodevelopment.Frontiers in molecular neuroscience · 2025Review
- Research advances of polycomb group proteins in regulating mammalian development.Frontiers in cell and developmental biology · 2024Review
- The function of histone methyltransferase SETDB1 and its roles in liver cancer.Frontiers in cell and developmental biology · 2024Review
- Post-translational modifications of histones: Mechanisms, biological functions, and therapeutic targets.MedComm · 2023Review
- DAXX adds a de novo H3.3K9me3 deposition pathway to the histone chaperone network.Molecular cell · 2023Article
- SETDB1 regulates microtubule dynamics.Cell proliferation · 2022Article
- Long noncoding RNAGenes & diseases · 2022Review
- Maternal SMCHD1 regulates Hox gene expression and patterning in the mouse embryo.Nature communications · 2022Article
- Maternal SMCHD1 controls both imprinted Xist expression and imprinted X chromosome inactivation.Epigenetics & chromatin · 2022Article
- The Molecular and Nuclear Dynamics of X-Chromosome Inactivation.Cold Spring Harbor perspectives in biology · 2022Review
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Authors and funding
20 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe presence of histone 3 lysine 9 (H3K9) methylation on the mouse inactive X chromosome has been controversial over the last 15 years, and the functional role of H3K9 methylation in X chromosome inactivation in any species has remained largely unexplored.
resultsHere we report the first genomic analysis of H3K9 di- and tri-methylation on the inactive X: we find they are enriched at the intergenic, gene poor regions of the inactive X, interspersed between H3K27 tri-methylation domains found in the gene dense regions. Although H3K9 methylation is predominantly non-genic, we find that depletion of H3K9 methylation via depletion of H3K9 methyltransferase Set domain bifurcated 1 (Setdb1) during the establishment of X inactivation, results in failure of silencing for around 150 genes on the inactive X. By contrast, we find a very minor role for Setdb1-mediated H3K9 methylation once X inactivation is fully established. In addition to failed gene silencing, we observed a specific failure to silence X-linked long-terminal repeat class repetitive elements.
conclusionsHere we have shown that H3K9 methylation clearly marks the murine inactive X chromosome. The role of this mark is most apparent during the establishment phase of gene silencing, with a more muted effect on maintenance of the silent state. Based on our data, we hypothesise that Setdb1-mediated H3K9 methylation plays a role in epigenetic silencing of the inactive X via silencing of the repeats, which itself facilitates gene silencing through alterations to the conformation of the whole inactive X chromosome.
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