ArticleMolecular and cellular biology2003
Direct repression of splicing by transformer-2.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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
15 citing papers in PubMed, 24 citations in OpenAlex.
- Perspective in Alternative Splicing Coupled to Nonsense-Mediated mRNA Decay.International journal of molecular sciences · 2020Review
- The Nix locus on the male-specific homologue of chromosome 1 in Aedes albopictus is a strong candidate for a male-determining factor.Parasites & vectors · 2018Article
- Article
- Tethered Function Assays as Tools to Elucidate the Molecular Roles of RNA-Binding Proteins.Advances in experimental medicine and biology · 2016Article
- Human Tra2 proteins jointly control a CHEK1 splicing switch among alternative and constitutive target exons.Nature communications · 2014Article
- Tribolium castaneum Transformer-2 regulates sex determination and development in both males and females.Insect biochemistry and molecular biology · 2013Article
- Half pint/Puf68 is required for negative regulation of splicing by the SR splicing factor Transformer2.RNA biology · 2013Article
- Activation and repression functions of an SR splicing regulator depend on exonic versus intronic-binding position.Nucleic acids research · 2012Article
- Regulated functional alternative splicing in Drosophila.Nucleic acids research · 2012Review
- Competing upstream 5' splice sites enhance the rate of proximal splicing.Molecular and cellular biology · 2010Article
- Control of alternative splicing by signal-dependent degradation of splicing-regulatory proteins.The Journal of biological chemistry · 2009Article
- The doublesex splicing enhancer components Tra2 and Rbp1 also repress splicing through an intronic silencer.Molecular and cellular biology · 2007Article
- Identification of a splicing enhancer in MLH1 using COMPARE, a new assay for determination of relative RNA splicing efficiencies.Human molecular genetics · 2006Article
- Concentration dependent selection of targets by an SR splicing regulator results in tissue-specific RNA processing.Nucleic acids research · 2006Article
- Sex determination in Drosophila melanogaster and Musca domestica converges at the level of the terminal regulator doublesex.Development genes and evolution · 2004Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The Drosophila melanogaster sex determination factor Tra2 positively regulates the splicing of both doublesex (dsx) and fruitless (fru) pre-mRNAs but negatively affects the splicing of the M1 intron in tra2 pre-mRNA. Retention of the M1 intron is known to be part of a negative-feedback mechanism wherein the Tra2 protein limits its own synthesis, but the mechanism responsible for accumulation of M1-containing RNA is unknown. Here we show that the recombinant Tra2 protein specifically represses M1 splicing in Drosophila nuclear extracts. We find that the Tra2 protein binds directly to several sites in and near the M1 intron and that, when Tra2 binding is competed with other RNAs, the splicing of M1 is restored. Mapping the RNA sequences functionally required for M1 repression identified both a 34-nucleotide (nt) A/C-rich sequence immediately upstream of the M1 5' splice site and a region within the intron itself. The AC-rich sequence is largely composed of a repeated 4-nt sequence that also forms a subrepeat within the repeated 13-nt splicing enhancer elements of fru and dsx RNAs. Although required for repression, the element also enhances M1 splicing in the absence of Tra2. We propose that Tra2 represses M1 splicing by interacting with multiple sequences in the pre-mRNA and interfering with enhancer function.
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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.