ArticleRNA (New York, N.Y.)2011
Contribution of base-pairing interactions between group II intron fragments during trans-splicing in vivo.
Article in RNA (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Group I Intron as a Potential Target for Antifungal Compounds: Development of aMolecules (Basel, Switzerland) · 2023Article
- Programmable Genome Editing Tools and their Regulation for Efficient Genome Engineering.Computational and structural biotechnology journal · 2017Review
- Circularization pathway of a bacterial group II intron.Nucleic acids research · 2016Article
- Using Group II Introns for Attenuating the In Vitro and In Vivo Expression of a Homing Endonuclease.PloS one · 2016Article
- Mobile Bacterial Group II Introns at the Crux of Eukaryotic Evolution.Microbiology spectrum · 2015Review
- Bacterial cellular engineering by genome editing and gene silencing.International journal of molecular sciences · 2014Review
- Isolation and characterization of functional tripartite group II introns using a Tn5-based genetic screen.PloS one · 2012Article
Corrections and comments
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Authors and funding
5 authors.
Funding
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Abstract
Group II introns are mobile genetic elements that self-splice from pre-mRNA transcripts. Some fragmented group II introns found in chloroplastic and mitochondrial genomes are able to assemble and splice in trans. The Ll.LtrB group II intron from the Gram-positive bacterium Lactococcus lactis was shown to splice in trans when fragmented at various locations throughout its structure. Here we used Ll.LtrB to assess the contribution of base-pairing interactions between intron fragments during trans-splicing in vivo. By comparing closely located fragmentation sites, we show that Ll.LtrB trans-splices more efficiently when base-pairing interactions can occur between the two intron fragments. Disruptions and stepwise restorations of specific base-pairing interactions between intron fragments resulted respectively in significant reductions and recoveries of the Ll.LtrB trans-splicing efficiency. Finally, although we confirm that LtrA is an important co-factor for trans-splicing, its overexpression cannot compensate for the reduction in trans-splicing efficiency when the potential base-pairing interactions between intron fragments are disrupted. These findings demonstrate the important contribution of base-pairing interactions for the assembly of group II intron fragments during trans-splicing and rationalizes why such interactions were evolutionarily conserved in natural trans-splicing group II introns.
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