ArticleFrontiers in genetics2021
U5 snRNA Interactions With Exons Ensure Splicing Precision.
Article in Frontiers in genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 18 citations in OpenAlex.
- Deployment of non-canonical splicing in tunicate genomes is mediated by divergent U2AF function and changing m6A modification in U1 and U6 snRNA.Nucleic acids research · 2026Article
- Prp16 enables efficient splicing of introns with diverse exonic consensus elements in the short-intron richRNA biology · 2025Article
- AProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Dominant variants in major spliceosome U4 and U5 small nuclear RNA genes cause neurodevelopmental disorders through splicing disruption.Nature genetics · 2025Article
- Analysis of R-loop forming regions identifies RNU2-2 and RNU5B-1 as neurodevelopmental disorder genes.Nature genetics · 2025Article
- RNA splicing: a split consensus reveals two major 5' splice site classes.Open biology · 2025Review
- Taxonomy of introns and the evolution of minor introns.Nucleic acids research · 2024Article
- Splicing analysis of STAT3 tandem donor suggests non-canonical binding registers for U1 and U6 snRNAs.Nucleic acids research · 2024Article
- Conserved and divergent signals in 5' splice site sequences across fungi, metazoa and plants.PLoS computational biology · 2023Article
- meLife · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Imperfect conservation of human pre-mRNA splice sites is necessary to produce alternative isoforms. This flexibility is combined with the precision of the message reading frame. Apart from intron-termini GU_AG and the branchpoint A, the most conserved are the exon-end guanine and +5G of the intron start. Association between these guanines cannot be explained solely by base-pairing with U1 snRNA in the early spliceosome complex. U6 succeeds U1 and pairs +5G in the pre-catalytic spliceosome, while U5 binds the exon end. Current U5 snRNA reconstructions by CryoEM cannot explain the conservation of the exon-end G. Conversely, human mutation analyses show that guanines of both exon termini can suppress splicing mutations. Our U5 hypothesis explains the mechanism of splicing precision and the role of these conserved guanines in the pre-catalytic spliceosome. We propose: (1) optimal binding register for human exons and U5-the exon junction positioned at U5Loop1 C
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