ArticlePLoS pathogens2014
Recruitment of RED-SMU1 complex by Influenza A Virus RNA polymerase to control Viral mRNA splicing.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 64 citations in OpenAlex.
- Human MX1 orchestrates the cytoplasmic sequestration of neosynthesized influenza A virus vRNPs.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Influenza A virus RNA localisation and the interceding trafficking pathways of the host cell.PLoS pathogens · 2025Review
- The RBPome of influenza A virus NP-mRNA reveals a role for TDP-43 in viral replication.Nucleic acids research · 2024Article
- Cryo-EM analyses of dimerized spliceosomes provide new insights into the functions of B complex proteins.The EMBO journal · 2024Article
- The host RNA polymerase II C-terminal domain is the anchor for replication of the influenza virus genome.Nature communications · 2024Article
- Applying Reverse Genetics to Study Measles Virus Interactions with the Host.Methods in molecular biology (Clifton, N.J.) · 2024Article
- SRSF5-Mediated Alternative Splicing of M Gene is Essential for Influenza A Virus Replication: A Host-Directed Target Against Influenza Virus.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Article
- Viral-host interactions during splicing and nuclear export of influenza virus mRNAs.Current opinion in virology · 2022Review
- H1N1 Influenza Virus-Infected Nasal Mucosal Epithelial Progenitor Cells Promote Dendritic Cell Recruitment and Maturation.Frontiers in immunology · 2022Article
- A Review and Meta-Analysis of Influenza Interactome Studies.Frontiers in microbiology · 2022Review
- Loss of splicing factor IK impairs normal skeletal muscle development.BMC biology · 2021Article
- Experimental Approaches to Identify Host Factors Important for Influenza Virus.Cold Spring Harbor perspectives in medicine · 2020Review
- Influenza virus infection induces widespread alterations of host cell splicing.NAR genomics and bioinformatics · 2020Article
- An SMU Splicing Factor Complex Within Nuclear Speckles Contributes to Magnesium Homeostasis in Arabidopsis.Plant physiology · 2020Article
- Human TRA2A determines influenza A virus host adaptation by regulating viral mRNA splicing.Science advances · 2020Article
- Alternative Experimental Models for Studying Influenza Proteins, Host-Virus Interactions and Anti-Influenza Drugs.Pharmaceuticals (Basel, Switzerland) · 2019Review
- RNA regulatory processes in RNA virus biology.Wiley interdisciplinary reviews. RNA · 2019Review
- Smu1 and RED are required for activation of spliceosomal B complexes assembled on short introns.Nature communications · 2019Article
- Destabilization of the human RED-SMU1 splicing complex as a basis for host-directed antiinfluenza strategy.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A viruses are major pathogens in humans and in animals, whose genome consists of eight single-stranded RNA segments of negative polarity. Viral mRNAs are synthesized by the viral RNA-dependent RNA polymerase in the nucleus of infected cells, in close association with the cellular transcriptional machinery. Two proteins essential for viral multiplication, the exportin NS2/NEP and the ion channel protein M2, are produced by splicing of the NS1 and M1 mRNAs, respectively. Here we identify two human spliceosomal factors, RED and SMU1, that control the expression of NS2/NEP and are required for efficient viral multiplication. We provide several lines of evidence that in infected cells, the hetero-trimeric viral polymerase recruits a complex formed by RED and SMU1 through interaction with its PB2 and PB1 subunits. We demonstrate that the splicing of the NS1 viral mRNA is specifically affected in cells depleted of RED or SMU1, leading to a decreased production of the spliced mRNA species NS2, and to a reduced NS2/NS1 protein ratio. In agreement with the exportin function of NS2, these defects impair the transport of newly synthesized viral ribonucleoproteins from the nucleus to the cytoplasm, and strongly reduce the production of infectious influenza virions. Overall, our results unravel a new mechanism of viral subversion of the cellular splicing machinery, by establishing that the human splicing factors RED and SMU1 act jointly as key regulators of influenza virus gene expression. In addition, our data point to a central role of the viral RNA polymerase in coupling transcription and alternative splicing of the viral mRNAs.
Indexed as
Identifiers
What OpenQuestion holds
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.