ArticleGenes & development2014
HIRA orchestrates a dynamic chromatin landscape in senescence and is required for suppression of neoplasia.
Article in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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Who cites it
104 citing papers in PubMed, 162 citations in OpenAlex.
- Microglia activation by derepression of endogenous retroviruses drives inflammation and cellular senescence.Nature neuroscience · 2026Article
- SenFlag gene signature identifies senescent cells in mouse and human tissues through a conserved core transcriptional program.The EMBO journal · 2026Article
- Senescent cells cluster CTCF on nuclear speckles to instruct an alternative splicing program.Nature aging · 2026Article
- HIRA-mediated H3.3 deposition preserves hepatocyte cell identity during liver aging.Research square · 2026Article
- HIRA-SETDB1-H3K9me3 axis regulates chromatin architecture in leukemia cells.The Journal of biological chemistry · 2026Article
- Histone variant H2A.Z mutant suppresses the senescence-associated secretory phenotype.bioRxiv : the preprint server for biology · 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
- Article
- Nucleosome stability safeguards cell identity, stress resilience and healthy aging.bioRxiv : the preprint server for biology · 2025Article
- Interrogating the regulatory epigenome of cellular senescence.Cellular and molecular life sciences : CMLS · 2025Review
- Targeting CyclinD1-CDK6 to Mitigate Senescence-Driven Inflammation and Age-Associated Functional Decline.bioRxiv : the preprint server for biology · 2025Article
- A transcriptome-based human universal senescence index (hUSI) robustly predicts cellular senescence under various conditions.Nature aging · 2025Article
- Deepening the Modulatory Activity of Bioactive Compounds Against AFB1- and OTA-Induced Neuronal Toxicity Through a Proteomic Approach.Antioxidants (Basel, Switzerland) · 2025Article
- Sendotypes predict worsening renal function in chronic kidney disease patients.Clinical and translational medicine · 2025Article
- In Situ and In Silico Methods for Senescence Identification in Human Liver Diseases.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Differential modulation of polycomb-associated histone marks by cBAF, pBAF, and gBAF complexes.Life science alliance · 2024Article
- The role of the dynamic epigenetic landscape in senescence: orchestrating SASP expression.npj aging · 2024Review
- SRSF6 modulates histone-chaperone HIRA splicing to orchestrate AR and E2F activity in prostate cancer.Science advances · 2024Article
- Article
- Histone chaperone HIRA, promyelocytic leukemia protein, and p62/SQSTM1 coordinate to regulate inflammation during cell senescence.Molecular cell · 2024Article
44 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors at 2 institutions in 1 country.
Funding
Abstract
Cellular senescence is a stable proliferation arrest that suppresses tumorigenesis. Cellular senescence and associated tumor suppression depend on control of chromatin. Histone chaperone HIRA deposits variant histone H3.3 and histone H4 into chromatin in a DNA replication-independent manner. Appropriately for a DNA replication-independent chaperone, HIRA is involved in control of chromatin in nonproliferating senescent cells, although its role is poorly defined. Here, we show that nonproliferating senescent cells express and incorporate histone H3.3 and other canonical core histones into a dynamic chromatin landscape. Expression of canonical histones is linked to alternative mRNA splicing to eliminate signals that confer mRNA instability in nonproliferating cells. Deposition of newly synthesized histones H3.3 and H4 into chromatin of senescent cells depends on HIRA. HIRA and newly deposited H3.3 colocalize at promoters of expressed genes, partially redistributing between proliferating and senescent cells to parallel changes in expression. In senescent cells, but not proliferating cells, promoters of active genes are exceptionally enriched in H4K16ac, and HIRA is required for retention of H4K16ac. HIRA is also required for retention of H4K16ac in vivo and suppression of oncogene-induced neoplasia. These results show that HIRA controls a specialized, dynamic H4K16ac-decorated chromatin landscape in senescent cells and enforces tumor suppression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.