ArticleRNA (New York, N.Y.)2010
Genetic identification of potential RNA-binding regions in a group II intron-encoded reverse transcriptase.
Article in RNA (New York, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Rewriting the genome: harnessing R2 retrotransposons for precise DNA insertion.Frontiers in genome editing · 2026Review
- Cysteine Mutagenesis of a Group II Intron-Encoded Protein Supports Splicing, Mobility, and Site-Specific Labeling.Biochemistry · 2025Article
- Structural basis for the evolution of a domesticated group II intron-like reverse transcriptase to function in host cell DNA repair.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Exon and protein positioning in a pre-catalytic group II intron RNP primed for splicing.Nucleic acids research · 2020Article
- Unraveling the role of the enigmatic MatK maturase in chloroplast group IIA intron excision.Plant direct · 2020Article
- Group II Intron RNPs and Reverse Transcriptases: From Retroelements to Research Tools.Cold Spring Harbor perspectives in biology · 2019Review
- The group II intron maturase: a reverse transcriptase and splicing factor go hand in hand.Current opinion in structural biology · 2017Review
- Structural Insights into the Mechanism of Group II Intron Splicing.Trends in biochemical sciences · 2017Review
- Globular domain structure and function of restriction-like-endonuclease LINEs: similarities to eukaryotic splicing factor Prp8.Mobile DNA · 2017Article
- Crystal structures of a group II intron maturase reveal a missing link in spliceosome evolution.Nature structural & molecular biology · 2016Article
- Structure of a group II intron in complex with its reverse transcriptase.Nature structural & molecular biology · 2016Article
- Functionality ofFrontiers in molecular biosciences · 2016Article
- Integration, Regulation, and Long-Term Stability of R2 Retrotransposons.Microbiology spectrum · 2015Review
- Mobile Bacterial Group II Introns at the Crux of Eukaryotic Evolution.Microbiology spectrum · 2015Review
- Identification of RNA binding motifs in the R2 retrotransposon-encoded reverse transcriptase.Nucleic acids research · 2014Article
- Article
- Article
- Group II introns: mobile ribozymes that invade DNA.Cold Spring Harbor perspectives in biology · 2011Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Mobile group II introns encode a reverse transcriptase that binds the intron RNA to promote RNA splicing and intron mobility, the latter via reverse splicing of the excised intron into DNA sites, followed by reverse transcription. Previous work showed that the Lactococcus lactis Ll.LtrB intron reverse transcriptase, denoted LtrA protein, binds with high affinity to DIVa, a stem-loop structure at the beginning of the LtrA open reading frame and makes additional contacts with intron core regions that stabilize the active RNA structure for forward and reverse splicing. LtrA's binding to DIVa down-regulates its translation and is critical for initiation of reverse transcription. Here, by using high-throughput unigenic evolution analysis with a genetic assay in which LtrA binding to DIVa down-regulates translation of GFP, we identified regions at LtrA's N terminus that are required for DIVa binding. Then, by similar analysis with a reciprocal genetic assay, we confirmed that residual splicing of a mutant intron lacking DIVa does not require these N-terminal regions, but does require other reverse transcriptase (RT) and X/thumb domain regions that bind the intron core. We also show that N-terminal fragments of LtrA by themselves bind specifically to DIVa in vivo and in vitro. Our results suggest a model in which the N terminus of nascent LtrA binds DIVa of the intron RNA that encoded it and nucleates further interactions with core regions that promote RNP assembly for RNA splicing and intron mobility. Features of this model may be relevant to evolutionarily related non-long-terminal-repeat (non-LTR)-retrotransposon RTs.
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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.