ArticleeLife2022
Dual signaling via interferon and DNA damage response elicits entrapment by giant PML nuclear bodies.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- PXL: a nucleic acid-binding module of the promyelocytic leukemia protein.Nucleic acids research · 2026Article
- DNA damage responses in HCMV infection: emerging mechanisms and outstanding questions.Journal of virology · 2026Review
- Non-canonical histone H3.3 and its chaperones HIRA and DAXX participate in the regulation of KSHV latency.bioRxiv : the preprint server for biology · 2026Article
- Review
- PXL: a Nucleic Acid-Binding Module of Promyelocytic Leukemia Protein.bioRxiv : the preprint server for biology · 2026Article
- Lytic or Latent Phase in Human Cytomegalovirus Infection: An Epigenetic Trigger.International journal of molecular sciences · 2025Review
- Manipulation of Nuclear-Related Pathways During Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication.Viruses · 2025Review
- Repression of varicella zoster virus gene expression during quiescent infection in the absence of detectable histone deposition.PLoS pathogens · 2025Article
- Membraneless organelles in health and disease: exploring the molecular basis, physiological roles and pathological implications.Signal transduction and targeted therapy · 2024Review
- Inhibition of human cytomegalovirus replication by interferon alpha can involve multiple anti-viral factors.The Journal of general virology · 2023Article
- Review
- Single-Cell, High-Content Microscopy Analysis of BK Polyomavirus Infection.Microbiology spectrum · 2023Article
- Article
- Promyelocytic Leukemia Protein Potently Restricts Human Cytomegalovirus Infection in Endothelial Cells.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PML nuclear bodies (PML-NBs) are dynamic interchromosomal macromolecular complexes implicated in epigenetic regulation as well as antiviral defense. During herpesvirus infection, PML-NBs induce epigenetic silencing of viral genomes, however, this defense is antagonized by viral regulatory proteins such as IE1 of human cytomegalovirus (HCMV). Here, we show that PML-NBs undergo a drastic rearrangement into highly enlarged PML cages upon infection with IE1-deficient HCMV. Importantly, our results demonstrate that dual signaling by interferon and DNA damage response is required to elicit giant PML-NBs. DNA labeling revealed that invading HCMV genomes are entrapped inside PML-NBs and remain stably associated with PML cages in a transcriptionally repressed state. Intriguingly, by correlative light and transmission electron microscopy (EM), we observed that PML cages also entrap newly assembled viral capsids demonstrating a second defense layer in cells with incomplete first-line response. Further characterization by 3D EM showed that hundreds of viral capsids are tightly packed into several layers of fibrous PML. Overall, our data indicate that giant PML-NBs arise via combined interferon and DNA damage signaling which triggers entrapment of both nucleic acids and proteinaceous components. This represents a multilayered defense strategy to act in a cytoprotective manner and to combat viral infections.
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Registered trials
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.