ArticleBMC biology2018
UBN1/2 of HIRA complex is responsible for recognition and deposition of H3.3 at cis-regulatory elements of genes in mouse ES cells.
Article in BMC biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 49 citations in OpenAlex.
- Histone H3 availability is more important for development than H3.2 versus H3.3 subtype identity.bioRxiv : the preprint server for biology · 2026Article
- The histone variant H3.14 is an early player in the abiotic stress response of Arabidopsis.Developmental cell · 2025Article
- Phosphorylation of H3.3 at Serine 31 acts as a switch of nucleosome dynamics for transcription.Nucleic acids research · 2025Article
- Histone variants: expanding the epigenetic potential of neurons one amino acid at a time.Trends in biochemical sciences · 2025Review
- Ubinuclein 2 is essential for mouse development and functions in X chromosome inactivation.PLoS genetics · 2025Article
- Single amino acid mutations in histone H3.3 illuminate the functional significance of H3K4 methylation in plants.Nature communications · 2025Article
- The Hira complex regulates Gli3R-dependent transcription in Hedgehog signaling and medulloblastoma cell growth and migration.Scientific reports · 2025Article
- Histone 3.3-related chromatinopathy: missense variants throughout H3-3A and H3-3B cause a range of functional consequences across species.Human genetics · 2024Review
- Alzheimer's Disease-Related Epigenetic Changes: Novel Therapeutic Targets.Molecular neurobiology · 2024Review
- HIRA vs. DAXX: the two axes shaping the histone H3.3 landscape.Experimental & molecular medicine · 2024Review
- Article
- Activation-induced cytidine deaminase an antibody diversification enzyme interacts with chromatin modifier UBN1 in B-cells.Scientific reports · 2023Article
- Histone Variants and Their Chaperones in Hematological Malignancies.HemaSphere · 2023Review
- Histone exchange sensors reveal variant specific dynamics in mouse embryonic stem cells.Nature communications · 2023Article
- Histone chaperone HIRA complex regulates retrotransposons in embryonic stem cells.Stem cell research & therapy · 2022Article
- HIRA complex presets transcriptional potential through coordinating depositions of the histone variants H3.3 and H2A.Z on the poised genes in mESCs.Nucleic acids research · 2022Article
- The ADAM9/UBN2/AKR1C3 axis promotes resistance to androgen-deprivation in prostate cancer.American journal of cancer research · 2022Article
- Dissecting regulatory pathways for transcription recovery following DNA damage reveals a non-canonical function of the histone chaperone HIRA.Nature communications · 2021Article
- Histone variants in skeletal myogenesis.Epigenetics · 2021Review
- Dynamic Activity of Histone H3-Specific Chaperone Complexes in Oncogenesis.Frontiers in oncology · 2021Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundH3.3 is an ancient and conserved H3 variant and plays essential roles in transcriptional regulation. HIRA complex, which is composed of HIRA, UBN1 or UBN2, and Cabin1, is a H3.3 specific chaperone complex. However, it still remains largely uncharacterized how HIRA complex specifically recognizes and deposits H3.3 to the chromatin, such as promoters and enhancers.
resultsIn this study, we demonstrate that the UBN1 or UBN2 subunit is mainly responsible for specific recognition and direct binding of H3.3 by the HIRA complex. While the HIRA subunit can enhance the binding affinity of UBN1 toward H3.3, Cabin1 subunit cannot. We also demonstrate that both Ala87 and Gly90 residues of H3.3 are required and sufficient for the specific recognition and binding by UBN1. ChIP-seq studies reveal that two independent HIRA complexes (UBN1-HIRA and UBN2-HIRA) can cooperatively deposit H3.3 to cis-regulatory regions, including active promoters and active enhancers in mouse embryonic stem (mES) cells. Importantly, disruption of histone chaperone activities of UBN1 and UBN2 by FID/AAA mutation results in the defect of H3.3 deposition at promoters of developmental genes involved in neural differentiation, and subsequently causes the failure of activation of these genes during neural differentiation of mES cells.
conclusionTogether, our results provide novel insights into the mechanism by which the HIRA complex specifically recognizes and deposits H3.3 at promoters and enhancers of developmental genes, which plays a critical role in neural differentiation of mES cells.
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