ArticleRNA (New York, N.Y.)2007
A dynamic bulge in the U6 RNA internal stem-loop functions in spliceosome assembly and activation.
Article in RNA (New York, N.Y.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Mechanism of spliceosome termination.Nature · 2026Article
- THUMPD2 catalyzes the N2-methylation of U6 snRNA of the spliceosome catalytic center and regulates pre-mRNA splicing and retinal degeneration.Nucleic acids research · 2024Article
- Thermodynamic examination of pH and magnesium effect on U6 RNA internal loop.RNA (New York, N.Y.) · 2019Article
- An Allosteric Network for Spliceosome Activation Revealed by High-Throughput Suppressor Analysis inGenetics · 2019Article
- The life of U6 small nuclear RNA, from cradle to grave.RNA (New York, N.Y.) · 2018Review
- Structural Roles of Noncoding RNAs in the Heart of Enzymatic Complexes.Biochemistry · 2017Article
- A multi-step model for facilitated unwinding of the yeast U4/U6 RNA duplex.Nucleic acids research · 2016Article
- Improved Model for Predicting the Free Energy Contribution of Dinucleotide Bulges to RNA Duplex Stability.Biochemistry · 2015Article
- Spliceosome assembly in the absence of stable U4/U6 RNA pairing.RNA (New York, N.Y.) · 2015Article
- Brr2 plays a role in spliceosomal activation in addition to U4/U6 unwinding.Nucleic acids research · 2015Article
- Improved model to predict the free energy contribution of trinucleotide bulges to RNA duplex stability.Biochemistry · 2014Article
- Core structure of the U6 small nuclear ribonucleoprotein at 1.7-Å resolution.Nature structural & molecular biology · 2014Article
- Comprehensive in vivo RNA-binding site analyses reveal a role of Prp8 in spliceosomal assembly.Nucleic acids research · 2013Article
- Cwc2 and its human homologue RBM22 promote an active conformation of the spliceosome catalytic centre.The EMBO journal · 2012Article
- Stem loop sequences specific to transposable element IS605 are found linked to lipoprotein genes in Borrelia plasmids.PloS one · 2009Article
- Minimum-energy path for a u6 RNA conformational change involving protonation, base-pair rearrangement and base flipping.Journal of molecular biology · 2009Article
- The PKR-binding domain of adenovirus VA RNAI exists as a mixture of two functionally non-equivalent structures.Nucleic acids research · 2009Article
- Intergenic regions of Borrelia plasmids contain phylogenetically conserved RNA secondary structure motifs.BMC genomics · 2009Article
- Computational identification of four spliceosomal snRNAs from the deep-branching eukaryote Giardia intestinalis.PloS one · 2008Article
- "Nought may endure but mutability": spliceosome dynamics and the regulation of splicing.Molecular cell · 2008Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The highly conserved internal stem-loop (ISL) of U6 spliceosomal RNA is unwound for U4/U6 complex formation during spliceosome assembly and reformed upon U4 release during spliceosome activation. The U6 ISL is structurally similar to Domain 5 of group II self-splicing introns, and contains a dynamic bulge that coordinates a Mg++ ion essential for the first catalytic step of splicing. We have analyzed the causes of growth defects resulting from mutations in the Saccharomyces cerevisiae U6 ISL-bulged nucleotide U80 and the adjacent C67-A79 base pair. Intragenic suppressors and enhancers of the cold-sensitive A79G mutation, which replaces the C-A pair with a C-G pair, suggest that it stabilizes the ISL, inhibits U4/U6 assembly, and may also disrupt spliceosome activation. The lethality of mutations C67A and C67G results from disruption of base-pairing potential between U4 and U6, as these mutations are fully suppressed by compensatory mutations in U4 RNA. Strikingly, suppressor analysis shows that the lethality of the U80G mutation is due not only to formation of a stable base pair with C67, as previously proposed, but also another defect. A U6-U80G strain in which mispairing with position 67 is prevented grows poorly and assembles aberrant spliceosomes that retain U1 snRNP and fail to fully unwind the U4/U6 complex at elevated temperatures. Our data suggest that the U6 ISL bulge is important for coupling U1 snRNP release with U4/U6 unwinding during spliceosome activation.
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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.