ArticleNucleic acids research2009
Limited complementarity between U1 snRNA and a retroviral 5' splice site permits its attenuation via RNA secondary structure.
Article in Nucleic acids research, 2009. 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, 25 citations in OpenAlex.
- RNA-interactome capture identifies SRSF3 as a key protein for herpesviral gene expression.PNAS nexus · 2025Article
- U1 snRNA interactions with deep intronic sequences regulate splicing of multiple exons of spinal muscular atrophy genes.Frontiers in neuroscience · 2024Article
- The HIV 5' Gag Region Displays a Specific Nucleotide Bias Regulating Viral Splicing and Infectivity.Viruses · 2021Article
- Analysis of Competing HIV-1 Splice Donor Sites Uncovers a Tight Cluster of Splicing Regulatory Elements within Exon 2/2b.Journal of virology · 2017Article
- HIV-1 Vpr N-terminal tagging affects alternative splicing of the viral genome.Scientific reports · 2016Article
- ORF57 overcomes the detrimental sequence bias of Kaposi's sarcoma-associated herpesvirus lytic genes.Journal of virology · 2015Article
- Identification of conserved RNA secondary structures at influenza B and C splice sites reveals similarities and differences between influenza A, B, and C.BMC research notes · 2014Article
- U1snRNP-mediated suppression of polyadenylation in conjunction with the RNA structure controls poly (A) site selection in foamy viruses.Retrovirology · 2013Article
- The 0.3-kb fragment containing the R-U5-5'leader sequence of Friend murine leukemia virus influences the level of protein expression from spliced mRNA.Virology journal · 2013Article
- A complex immunodeficiency is based on U1 snRNP-mediated poly(A) site suppression.The EMBO journal · 2012Article
- PSF suppresses tau exon 10 inclusion by interacting with a stem-loop structure downstream of exon 10.Journal of molecular neuroscience : MN · 2011Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple types of regulation are used by cells and viruses to control alternative splicing. In murine leukemia virus, accessibility of the 5' splice site (ss) is regulated by an upstream region, which can fold into a complex RNA stem-loop structure. The underlying sequence of the structure itself is negligible, since most of it could be functionally replaced by a simple heterologous RNA stem-loop preserving the wild-type splicing pattern. Increasing the RNA duplex formation between U1 snRNA and the 5'ss by a compensatory mutation in position +6 led to enhanced splicing. Interestingly, this mutation affects splicing only in the context of the secondary structure, arguing for a dynamic interplay between structure and primary 5'ss sequence. The reduced 5'ss accessibility could also be counteracted by recruiting a splicing enhancer domain via a modified MS2 phage coat protein to a single binding site at the tip of the simple RNA stem-loop. The mechanism of 5'ss attenuation was revealed using hyperstable U1 snRNA mutants, showing that restricted U1 snRNP access is the cause of retroviral alternative splicing.
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