ArticleMolecular and cellular biology2000
Binding of equine infectious anemia virus rev to an exon splicing enhancer mediates alternative splicing and nuclear export of viral mRNAs.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Review
- Identification of a Novel Post-transcriptional Transactivator from the Equine Infectious Anemia Virus.Journal of virology · 2022Article
- A Novel, Fully Spliced, Accessory Gene in Equine Lentivirus with Distinct Rev-Responsive Element.Journal of virology · 2022Article
- Structural Mimicry Drives HIV-1 Rev-Mediated HERV-K Expression.Journal of molecular biology · 2020Article
- Computational modeling suggests dimerization of equine infectious anemia virus Rev is required for RNA binding.Retrovirology · 2014Article
- Development of an equine-tropic replication-competent lentivirus assay for equine infectious anemia virus-based lentiviral vectors.Human gene therapy methods · 2012Article
- Rev variation during persistent lentivirus infection.Viruses · 2011Review
- Mapping of the functional boundaries and secondary structure of the mouse mammary tumor virus Rem-responsive element.The Journal of biological chemistry · 2009Article
- Article
- Equine infectious anemia virus resists the antiretroviral activity of equine APOBEC3 proteins through a packaging-independent mechanism.Journal of virology · 2008Article
- Article
- Characterization of functional domains of equine infectious anemia virus Rev suggests a bipartite RNA-binding domain.Journal of virology · 2006Article
- The retrovirus RNA trafficking granule: from birth to maturity.Retrovirology · 2006Review
- Subpopulations of equine infectious anemia virus Rev coexist in vivo and differ in phenotype.Journal of virology · 2003Article
- ZNF265--a novel spliceosomal protein able to induce alternative splicing.The Journal of cell biology · 2001Article
- Selective inhibition of splicing at the avian sarcoma virus src 3' splice site by direct-repeat posttranscriptional cis elements.Journal of virology · 2000Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
In addition to facilitating the nuclear export of incompletely spliced viral mRNAs, equine infectious anemia virus (EIAV) Rev regulates alternative splicing of the third exon of the tat/rev mRNA. In the presence of Rev, this exon of the bicistronic RNA is skipped in a fraction of the spliced mRNAs. In this report, the cis-acting requirements for exon 3 usage were correlated with sequences necessary for Rev binding and transport of incompletely spliced RNA. The presence of a purine-rich exon splicing enhancer (ESE) was required for exon 3 recognition, and the addition of Rev inhibited exon 3 splicing. Glutathione-S-transferase (GST)-Rev bound to probes containing the ESE, and mutation of GAA repeats to GCA within the ESE inhibited both exon 3 recognition in RNA splicing experiments and GST-Rev binding in vitro. These results suggest that Rev regulates alternative splicing by binding at or near the ESE to block SR protein-ESE interactions. A 57-nucleotide sequence containing the ESE was sufficient to mediate Rev-dependent nuclear export of incompletely spliced RNAs. Rev export activity was significantly inhibited by mutation of the ESE or by trans-complementation with SF2/ASF. These results indicate that the ESE functions as a Rev-responsive element and demonstrate that EIAV Rev mediates exon 3 exclusion through protein-RNA interactions required for efficient export of incompletely spliced viral RNAs.
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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.