ArticlePLoS pathogens2018
HSV-1-induced disruption of transcription termination resembles a cellular stress response but selectively increases chromatin accessibility downstream of genes.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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71 citing papers in PubMed, 102 citations in OpenAlex.
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- Regulation of gene expression by alternative polyadenylation in health and disease.Nature reviews. Genetics · 2026Review
- Resolving human neuronal herpesvirus reactivation via petabase-scale association studies.bioRxiv : the preprint server for biology · 2026Article
- The Goldilocks state of transcriptional readthrough for chimeric splicing.Transcription · 2026Review
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- Identity rather than 3D position informs splicing of rare introns in the human genome.iScience · 2026Article
- Dynamic chromatin accessibility and transcriptional landscapes of porcine kidney cells during pseudorabies virus infection.Frontiers in immunology · 2026Article
- Base Composition Influences the Position and Precision of RNA Polymerase II Disassociation in Basal and Perturbed Conditions.bioRxiv : the preprint server for biology · 2025Article
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- Transcriptional readthrough precedes alternative splicing programs triggered in CML cells by imatinib.bioRxiv : the preprint server for biology · 2025Article
- Dual roles of NScience China. Life sciences · 2025Article
- Regulatory Mechanisms and Functional Roles of Readthrough Transcripts in Tumorigenesis.International journal of molecular sciences · 2025Review
- Oncogenic roles of young human de novo genes and their potential as neoantigens in cancer immunotherapy.Cell genomics · 2025Article
- Microtubule mechanotransduction refines cytomegalovirus interactions with and remodeling of host chromatin.Nature communications · 2025Article
- Comprehensive resource for transcription readthrough events in healthy human tissues.Scientific data · 2025Article
- Herpes simplex virus type 1 reshapes host chromatin architecture via transcription machinery hijacking.Nature communications · 2025Article
- HSV-1 infection induces a downstream shift of the +1 nucleosome.Journal of virology · 2025Article
- Herpesviruses mimic zygotic genome activation to promote viral replication.Nature communications · 2025Article
- Fateful Decisions of Where to Cut the Line: Pathology Associated with Aberrant 3' End Processing and Transcription Termination.Journal of molecular biology · 2025Review
11 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lytic herpes simplex virus 1 (HSV-1) infection triggers disruption of transcription termination (DoTT) of most cellular genes, resulting in extensive intergenic transcription. Similarly, cellular stress responses lead to gene-specific transcription downstream of genes (DoG). In this study, we performed a detailed comparison of DoTT/DoG transcription between HSV-1 infection, salt and heat stress in primary human fibroblasts using 4sU-seq and ATAC-seq. Although DoTT at late times of HSV-1 infection was substantially more prominent than DoG transcription in salt and heat stress, poly(A) read-through due to DoTT/DoG transcription and affected genes were significantly correlated between all three conditions, in particular at earlier times of infection. We speculate that HSV-1 either directly usurps a cellular stress response or disrupts the transcription termination machinery in other ways but with similar consequences. In contrast to previous reports, we found that inhibition of Ca2+ signaling by BAPTA-AM did not specifically inhibit DoG transcription but globally impaired transcription. Most importantly, HSV-1-induced DoTT, but not stress-induced DoG transcription, was accompanied by a strong increase in open chromatin downstream of the affected poly(A) sites. In its extent and kinetics, downstream open chromatin essentially matched the poly(A) read-through transcription. We show that this does not cause but rather requires DoTT as well as high levels of transcription into the genomic regions downstream of genes. This raises intriguing new questions regarding the role of histone repositioning in the wake of RNA Polymerase II passage downstream of impaired poly(A) site recognition.
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