ArticleNature structural & molecular biology2025
Heritable maintenance of chromatin modifications confers transcriptional memory of interferon-γ signaling.
Article in Nature structural & molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- The effects of IFNγ on tissue physiology through structural cells.Nature reviews. Immunology · 2026Review
- Heritable single-cell gene expression states shape functional variability in innate immune responses.bioRxiv : the preprint server for biology · 2026Article
- Review
- IFNγ blockade in Mycobacterium tuberculosis infected macaques alters the granuloma environment but not bacterial control.Nature communications · 2026Article
- IFNγ-induced memory in human macrophages is sustained by the durability of cytokine signaling itself.The Journal of experimental medicine · 2026Article
- Sequential RNA polymerase II activation drives human hematopoiesis.Cell reports · 2026Article
- Rare epigenetic alterations are conserved across hematopoietic differentiation stages after mycobacterial infection.JCI insight · 2026Article
- Integrated multi-omics analysis reveals shared IFN-γ-associated monocyte signatures in primary Sjögren's syndrome and Alzheimer's disease.Frontiers in immunology · 2026Article
- Dynamic Balance of Histone H3 Methylation: Regulatory Mechanisms and Therapeutic Prospects in RA Immune Dysregulation and Bone Metabolism Imbalance.Journal of immunology research · 2026Review
- Immune signaling as a determinant of cellular identity and tissue function.Frontiers in immunology · 2026Review
- Innate immune sensing and signaling: Co-opted for genome surveillance? Implications for tumorigenesis.DNA repair · 2025Review
- The epigenetic circle: feedback loops in the maintenance of cellular memory.Epigenetics & chromatin · 2025Review
- The yin yang of transcriptional memory.Nature structural & molecular biology · 2025Article
- Long-term memory in epithelia: transient IFNγ exposure drives stable repression of TFF1 in gastric epithelial cells via epigenetic changes.Frontiers in immunology · 2025Article
- New insights into coordinated regulation of AHR promoter transcription; molecular mechanisms and therapeutic targets.International journal of biological sciences · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Interferon-γ (IFNγ) transiently activates genes related to inflammation and innate immunity. A subset of targets retain a mitotically heritable memory of prior IFNγ exposure, resulting in hyperactivation upon re-exposure through poorly understood mechanisms. Here, we discover that the transcriptionally permissive chromatin marks H3K4me1, H3K14ac and H4K16ac are established during IFNγ priming and are selectively maintained on a cluster of guanylate-binding protein (GBP) genes in dividing human cells in the absence of transcription. The histone acetyltransferase KAT7 is required for H3K14ac deposition at GBP genes and for accelerated GBP reactivation upon re-exposure to IFNγ. In naive cells, the GBP cluster is maintained in a low-level repressive chromatin state, marked by H3K27me3, limiting priming through a PRC2-dependent mechanism. Unexpectedly, IFNγ priming results in transient accumulation of this repressive mark despite active gene expression. However, during the memory phase, H3K27 methylation is selectively depleted from primed GBP genes, facilitating hyperactivation. Furthermore, we identified a cis-regulatory element that forms transient, long-range contacts across the GBP cluster and acts as a repressor, curbing hyperactivation of previously IFNγ-primed cells. Our results provide insight into the chromatin basis for the long-term transcriptional memory of IFNγ signaling, which might contribute to enhanced innate immunity.
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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.