ArticleJournal of virology1995
A poliovirus 2A(pro) mutant unable to cleave 3CD shows inefficient viral protein synthesis and transactivation defects.
Article in Journal of virology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Review
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- Recent Progress on Functional Genomics Research of Enterovirus 71.Virologica Sinica · 2019Review
- Exploration of sequence space as the basis of viral RNA genome segmentation.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Deubiquitinase function of arterivirus papain-like protease 2 suppresses the innate immune response in infected host cells.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- The multifaceted poliovirus 2A protease: regulation of gene expression by picornavirus proteases.Journal of biomedicine & biotechnology · 2011Article
- HIV- 1 protease inhibits Cap- and poly(A)-dependent translation upon eIF4GI and PABP cleavage.PloS one · 2009Article
- Proteinase 2Apro is essential for enterovirus replication in type I interferon-treated cells.Journal of virology · 2009Article
- Viral translation is coupled to transcription in Sindbis virus-infected cells.Journal of virology · 2007Article
- Antiviral effect of the mammalian translation initiation factor 2alpha kinase GCN2 against RNA viruses.The EMBO journal · 2006Article
- Translational resistance of late alphavirus mRNA to eIF2alpha phosphorylation: a strategy to overcome the antiviral effect of protein kinase PKR.Genes & development · 2006Article
- The eukaryotic translation initiation factor 4GI is cleaved by different retroviral proteases.Journal of virology · 2003Article
- A stable HeLa cell line that inducibly expresses poliovirus 2A(pro): effects on cellular and viral gene expression.Journal of virology · 2000Article
- Cleavage of eukaryotic translation initiation factor 4G by exogenously added hybrid proteins containing poliovirus 2Apro in HeLa cells: effects on gene expression.Molecular and cellular biology · 1999Article
- Genetic selection of poliovirus 2Apro-binding peptides.Journal of virology · 1999Article
- Nitric oxide inhibition of coxsackievirus replication in vitro.The Journal of clinical investigation · 1997Article
- Viral cysteine proteinases.Perspectives in drug discovery and design : PD3 · 1996Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Four poliovirus mutants with modifications of tyrosine 88 in 2A(pro) were generated and introduced into the cloned poliovirus genome. Mutants Y88P and Y88L were nonviable, mutant Y88F showed a wild-type (WT) phenotype, and mutant Y88S showed a delayed cytopathic effect and formed small plaques in HeLa cells. Growth of Y88S in HeLa cells was restricted, giving rise to about 20% of the PFU production of the WT poliovirus. The 2A (Y88S) mutant synthesized significantly lower levels of viral proteins in HeLa cells than did the WT poliovirus, while the kinetics of p220 cleavage were identical for both viruses. Strikingly, the 2A (Y88S) mutant was unable to cleave 3CD, as shown by analysis of poliovirus proteins labeled with [35S]methionine or immunoblotted with a specific anti-3C serum. The ability of the Y88S mutant to form infectious virus and cleave 3CD can be complemented by the WT poliovirus. Synthesis of viral RNA was diminished in the Y88S mutant but less than the inhibition of translation of viral RNA. Experiments in which guanidine was used to inhibit poliovirus RNA synthesis suggest that the primary defect of the Y88S mutant virus is at the level of poliovirus RNA translation, while viral genome replication is much less affected. Transfection of HeLa cells infected with the WT poliovirus with a luciferase mRNA containing the poliovirus 5' untranslated sequence gives rise to a severalfold increase in luciferase activity. This enhanced translation of leader-luc mRNA was not observed when the transfected cells were infected with the 2A (Y88S) mutant. Moreover, cotransfection with mRNA encoding WT poliovirus 2A(pro) enhanced translation of leader-luc mRNA. This enhancement was much lower upon transfection with mRNA encoding 2A(Y88S), 2A(Y88L), or 2A(Y88P). These findings support the view that 2A(pro) itself, rather than the 3C' and/or 3D' products, is necessary for efficient translation of poliovirus RNA in HeLa cells.
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