ArticleNucleic acids research2022
Reovirus μ2 protein modulates host cell alternative splicing by reducing protein levels of U5 snRNP core components.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Nonsense-mediated decay controls a negative feedback loop in innate immune sensing.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Reovirus µ2 residue 208 drives SRSF2-dependent nuclear hyperaccumulation of IRF9.microPublication biology · 2026Article
- An overview of vital functions of human ecdysoneless (ECD), a highly conserved protein.Bioscience reports · 2025Review
- AProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Genome-wide association analysis of the resistance to infectious hematopoietic necrosis virus in two rainbow trout aquaculture lines confirms oligogenic architecture with several moderate effect quantitative trait loci.Frontiers in genetics · 2024Article
- Mechanisms of impairment of interferon production by SARS-CoV-2.Biochemical Society transactions · 2023Review
- Virus usurps alternative splicing to clear the decks for infection.Virology journal · 2023Review
- Reovirus Type 3 Dearing Variants Do Not Induce Necroptosis in RIPK3-Expressing Human Tumor Cell Lines.International journal of molecular sciences · 2023Article
- Plerixafor and resatorvid inhibit hepatitis B virusFrontiers in cellular and infection microbiology · 2023Article
- Reovirus μ2 Protein Impairs Translation to Reduce U5 snRNP Protein Levels.International journal of molecular sciences · 2022Article
- Article
- The μ2 and λ1 Proteins of Mammalian Reovirus Modulate Early Events Leading to Induction of the Interferon Signaling Network.Viruses · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Mammalian orthoreovirus (MRV) is a double-stranded RNA virus from the Reoviridae family presenting a promising activity as an oncolytic virus. Recent studies have underlined MRV's ability to alter cellular alternative splicing (AS) during infection, with a limited understanding of the mechanisms at play. In this study, we investigated how MRV modulates AS. Using a combination of cell biology and reverse genetics experiments, we demonstrated that the M1 gene segment, encoding the μ2 protein, is the primary determinant of MRV's ability to alter AS, and that the amino acid at position 208 in μ2 is critical to induce these changes. Moreover, we showed that the expression of μ2 by itself is sufficient to trigger AS changes, and its ability to enter the nucleus is not required for all these changes. Moreover, we identified core components of the U5 snRNP (i.e. EFTUD2, PRPF8, and SNRNP200) as interactors of μ2 that are required for MRV modulation of AS. Finally, these U5 snRNP components are reduced at the protein level by both MRV infection and μ2 expression. Our findings identify the reduction of U5 snRNP components levels as a new mechanism by which viruses alter cellular AS.
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