ArticlePLoS genetics2021
Mechanism and consequences of herpes simplex virus 1-mediated regulation of host mRNA alternative polyadenylation.
Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- Alpha-herpesvirus UL55 synergizes with ICP27 to suppress type I interferon production through conserved and host-adapted mechanisms.Journal of virology · 2026Article
- The competition between splicing and 3' processing shapes the human transcriptome.Genes & development · 2026Article
- Resolving human neuronal herpesvirus reactivation via petabase-scale association studies.bioRxiv : the preprint server for biology · 2026Article
- Regulation of gene expression by alternative polyadenylation in health and disease.Nature reviews. Genetics · 2026Review
- LENG8 mediates RNA nuclear retention and degradation in eukaryotes.Molecular cell · 2026Article
- HSV ICP27 hijacks host splicing factor SRSF3 to regulate pre-mRNA splicing and export for viral gene expression and immune evasion.PLoS pathogens · 2026Article
- PolyAseqTrap: a universal tool for genome-wide identification and quantification of polyadenylation sites from different 3' end sequencing data.Genome biology · 2026Article
- Antagonistic co-evolution throughout the herpesvirus life cycle.Virus evolution · 2026Review
- Alternative cleavage and polyadenylation: key regulatory mechanisms in health and disease.RNA biology · 2025Review
- A nuclear RNA degradation code is recognized by PAXT for eukaryotic transcriptome surveillance.Molecular cell · 2025Article
- RBBP6 anchors pre-mRNA 3' end processing to nuclear speckles for efficient gene expression.Molecular cell · 2025Article
- Fateful Decisions of Where to Cut the Line: Pathology Associated with Aberrant 3' End Processing and Transcription Termination.Journal of molecular biology · 2025Review
- U4 snRNP inhibits premature cleavage and polyadenylation of pre-mRNAs.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Aberrant RNA polymerase initiation and processivity on the genome of a herpes simplex virus 1 mutant lacking ICP27.Journal of virology · 2024Article
- Downregulation of CPSF6 leads to global mRNA 3' UTR shortening and enhanced antiviral immune responses.PLoS pathogens · 2024Article
- The anticancer compound JTE-607 reveals hidden sequence specificity of the mRNA 3' processing machinery.Nature structural & molecular biology · 2023Article
- A Recombinant Duck Plague Virus Containing the ICP27 Deletion Marker Provides Robust Protection in Ducks.Microbiology spectrum · 2023Article
- Knowing when to stop: Transcription termination on protein-coding genes by eukaryotic RNAPII.Molecular cell · 2023Review
- Emerging roles of alternative cleavage and polyadenylation (APA) in human disease.Journal of cellular physiology · 2022Review
- Control of animal virus replication by RNA adenosine methylation.Advances in virus research · 2022Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Eukaryotic gene expression is extensively regulated by cellular stress and pathogen infections. We have previously shown that herpes simplex virus 1 (HSV-1) and several cellular stresses cause widespread disruption of transcription termination (DoTT) of RNA polymerase II (RNAPII) in host genes and that the viral immediate early factor ICP27 plays an important role in HSV-1-induced DoTT. Here, we show that HSV-1 infection also leads to widespread changes in alternative polyadenylation (APA) of host mRNAs. In the majority of cases, polyadenylation shifts to upstream poly(A) sites (PAS), including many intronic PAS. Mechanistically, ICP27 contributes to HSV-1-mediated APA regulation. HSV-1- and ICP27-induced activation of intronic PAS is sequence-dependent and does not involve general inhibition of U1 snRNP. HSV1-induced intronic polyadenylation is accompanied by early termination of RNAPII. HSV-1-induced mRNAs polyadenylated at intronic PAS (IPA) are exported into the cytoplasm while APA isoforms with extended 3' UTRs are sequestered in the nuclei, both preventing the expression of the full-length gene products. Finally we provide evidence that HSV-induced IPA isoforms are translated. Together with other recent studies, our results suggest that viral infection and cellular stresses induce a multi-faceted host response that includes DoTT and changes in APA profiles.
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Registered trials
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