ArticleGenome biology2023
H3.3 contributes to chromatin accessibility and transcription factor binding at promoter-proximal regulatory elements in embryonic stem cells.
Article in Genome biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Identifying critical lysines in mammalian histone H3 with high-throughput CRISPR prime editing.Nature genetics · 2026Article
- DcH3.3 and DcNAC1 Regulate the Expression of UGT73A93 Involved in the Changes in Flower Colour and Fungal Resistance in Carnation.Plant biotechnology journal · 2026Article
- Histone H3.3 ensures cell proliferation and genomic stability during myeloid cell development.iScience · 2026Article
- ASF1B promotes erythropoiesis by regulating the establishment and enrichment of H3.3 nucleosomes.Nucleic acids research · 2026Article
- Defective plasticity in dermatomyositis patients muscle stem cells is associated with sustained intrinsic inflammatory signaling and disruption of the histone H3.3 chromatin loading pathway.NAR molecular medicine · 2026Article
- Histone H3 availability is more important for development than H3.2 versus H3.3 subtype identity.bioRxiv : the preprint server for biology · 2026Article
- Dynamic architecture of mammalian paternal chromatin: histone-to-protamine exchange and post-fertilization reprogramming.Epigenetics & chromatin · 2025Review
- Optimizing multifunctional fluorescent ligands for intracellular labeling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- ATRX Promotes Transcription Initiation of HSV-1 Immediate Early Genes During Early Lytic Infection.Viruses · 2025Article
- O-GlcNAcylation promotes angiogenic transdifferentiation to reverse vascular ischemia.Nature cardiovascular research · 2025Article
- Loss of ARID1A leads to a cold tumor phenotype via suppression of IFNγ signaling.Scientific reports · 2025Article
- Multifunctional histone variants in genome function.Nature reviews. Genetics · 2025Review
- The Mammalian Oocyte: A Central Hub for Cellular Reprogramming and Stemness.Stem cells and cloning : advances and applications · 2025Review
- The role of chromatin state in intron retention: A case study in leveraging large scale deep learning models.PLoS computational biology · 2025Article
- The cells are all-right: Regulation of the Lefty genes by separate enhancers in mouse embryonic stem cells.PLoS genetics · 2024Article
- Article
- H3.3K122A results in a neomorphic phenotype in mouse embryonic stem cells.Epigenetics & chromatin · 2024Article
- SRSF6 modulates histone-chaperone HIRA splicing to orchestrate AR and E2F activity in prostate cancer.Science advances · 2024Article
- H3.3K122A results in a neomorphic phenotype in mouse embryonic stem cells.Research square · 2024Article
- Plasma cell differentiation is regulated by the expression of histone variant H3.3.Nature communications · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe histone variant H3.3 is enriched at active regulatory elements such as promoters and enhancers in mammalian genomes. These regions are highly accessible, creating an environment that is permissive to transcription factor binding and the recruitment of transcriptional coactivators that establish a unique chromatin post-translational landscape. How H3.3 contributes to the establishment and function of chromatin states at these regions is poorly understood.
resultsWe perform genomic analyses of features associated with active promoter chromatin in mouse embryonic stem cells (ESCs) and find evidence of subtle yet widespread promoter dysregulation in the absence of H3.3. Loss of H3.3 results in reduced chromatin accessibility and transcription factor (TF) binding at promoters of expressed genes in ESCs. Likewise, enrichment of the transcriptional coactivator p300 and downstream histone H3 acetylation at lysine 27 (H3K27ac) is reduced at promoters in the absence of H3.3, along with reduced enrichment of the acetyl lysine reader BRD4. Despite the observed chromatin dysregulation, H3.3 KO ESCs maintain transcription from ESC-specific genes. However, upon undirected differentiation, H3.3 KO cells retain footprinting of ESC-specific TF motifs and fail to generate footprints of lineage-specific TF motifs, in line with their diminished capacity to differentiate.
conclusionsH3.3 facilitates DNA accessibility, transcription factor binding, and histone post-translational modification at active promoters. While H3.3 is not required for maintaining transcription in ESCs, it does promote de novo transcription factor binding which may contribute to the dysregulation of cellular differentiation in the absence of H3.3.
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