ArticlePLoS genetics2019
Lysine 27 of replication-independent histone H3.3 is required for Polycomb target gene silencing but not for gene activation.
Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- The histone code at a crossroads: history, context, and new approaches.Trends in genetics : TIG · 2026Review
- Epigenetic inheritance and gene expression regulation in early Drosophila embryos.EMBO reports · 2024Review
- Redesigning the Drosophila histone gene cluster: an improved genetic platform for spatiotemporal manipulation of histone function.Genetics · 2024Article
- Histone H3.3 lysine 9 and 27 control repressive chromatin at cryptic enhancers and bivalent promoters.Nature communications · 2024Article
- Article
- CBP and Gcn5 drive zygotic genome activation independently of their catalytic activity.Science advances · 2023Article
- Epigenetic moonlighting: Catalytic-independent functions of histone modifiers in regulating transcription.Science advances · 2023Review
- Acetylation of histone H2B marks active enhancers and predicts CBP/p300 target genes.Nature genetics · 2023Article
- Distinct roles for canonical and variant histone H3 lysine-36 in Polycomb silencing.Science advances · 2023Article
- H3.3 contributes to chromatin accessibility and transcription factor binding at promoter-proximal regulatory elements in embryonic stem cells.Genome biology · 2023Article
- Direct assessment of histone function using histone replacement.Trends in biochemical sciences · 2023Review
- Set2 family regulates mycotoxin metabolism and virulence via H3K36 methylation in pathogenic fungusVirulence · 2022Article
- Overlapping functions of RBBP4 and RBBP7 in regulating cell proliferation and histone H3.3 deposition during mouse preimplantation development.Epigenetics · 2022Article
- Histone editing elucidates the functional roles of H3K27 methylation and acetylation in mammals.Nature genetics · 2022Article
- Distinct developmental phenotypes result from mutation of Set8/KMT5A and histone H4 lysine 20 in Drosophila melanogaster.Genetics · 2022Article
- Multi-omic profiling of histone variant H3.3 lysine 27 methylation reveals a distinct role from canonical H3 in stem cell differentiation.Molecular omics · 2022Article
- Fasting drives the metabolic, molecular and geroprotective effects of a calorie-restricted diet in mice.Nature metabolism · 2021Article
- Polycomb-group recruitment to aScience advances · 2021Article
- Review
- Reevaluating the roles of histone-modifying enzymes and their associated chromatin modifications in transcriptional regulation.Nature genetics · 2020Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Proper determination of cell fates depends on epigenetic information that is used to preserve memory of decisions made earlier in development. Post-translational modification of histone residues is thought to be a central means by which epigenetic information is propagated. In particular, modifications of histone H3 lysine 27 (H3K27) are strongly correlated with both gene activation and gene repression. H3K27 acetylation is found at sites of active transcription, whereas H3K27 methylation is found at loci silenced by Polycomb group proteins. The histones bearing these modifications are encoded by the replication-dependent H3 genes as well as the replication-independent H3.3 genes. Owing to differential rates of nucleosome turnover, H3K27 acetylation is enriched on replication-independent H3.3 histones at active gene loci, and H3K27 methylation is enriched on replication-dependent H3 histones across silenced gene loci. Previously, we found that modification of replication-dependent H3K27 is required for Polycomb target gene silencing, but it is not required for gene activation. However, the contribution of replication-independent H3.3K27 to these functions is unknown. Here, we used CRISPR/Cas9 to mutate the endogenous replication-independent H3.3K27 to a non-modifiable residue. Surprisingly, we find that H3.3K27 is also required for Polycomb target gene silencing despite the association of H3.3 with active transcription. However, the requirement for H3.3K27 comes at a later stage of development than that found for replication-dependent H3K27, suggesting a greater reliance on replication-independent H3.3K27 in post-mitotic cells. Notably, we find no evidence of global transcriptional defects in H3.3K27 mutants, despite the strong correlation between H3.3K27 acetylation and active transcription.
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