ArticleRNA (New York, N.Y.)2007
An allosteric-feedback mechanism for protein-assisted group I intron splicing.
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 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- The Mrs1 splicing factor binds the bI3 group I intron at each of two tetraloop-receptor motifs.PloS one · 2010Article
- Global stabilization of rRNA structure by ribosomal proteins S4, S17, and S20.Journal of molecular biology · 2009Article
- Optimization of in vivo activity of a bifunctional homing endonuclease and maturase reverses evolutionary degradation.Nucleic acids research · 2009Article
- A DExH/D-box protein coordinates the two steps of splicing in a group I intron.Journal of molecular biology · 2008Article
- A shared RNA-binding site in the Pet54 protein is required for translational activation and group I intron splicing in yeast mitochondria.Nucleic acids research · 2008Article
- Evidence that binding of C5 protein to P RNA enhances ribozyme catalysis by influencing active site metal ion affinity.RNA (New York, N.Y.) · 2007Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The I-AniI maturase facilitates self-splicing of a mitochondrial group I intron in Aspergillus nidulans. Binding occurs in at least two steps: first, a specific but labile encounter complex rapidly forms and then this intermediate is slowly resolved into a native, catalytically active RNA/protein complex. Here we probe the structure of the RNA throughout the assembly pathway. Although inherently unstable, the intron core, when bound by I-AniI, undergoes rapid folding to a near-native state in the encounter complex. The next transition includes the slow destabilization and docking into the core of the peripheral stacked helix that contains the 5' splice site. Mutational analyses confirm that both transitions are important for native complex formation. We propose that protein-driven destabilization and docking of the peripheral stacked helix lead to subtle changes in the I-AniI binding site that facilitate native complex formation. These results support an allosteric-feedback mechanism of RNA-protein recognition in which proteins engaged in an intermediate complex can influence RNA structure far from their binding sites. The linkage of these changes to stable binding ensures that the protein and RNA do not get sequestered in nonfunctional complexes.
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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.