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The doublesex splicing enhancer components Tra2 and Rbp1 also repress splicing through an intronic silencer.

The doublesex splicing enhancer components Tra2 and Rbp1 also repress splicing through an intronic silencer. Research Abstract Details 

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  • The doublesex splicing enhancer components Tra2 and Rbp1 also repress splicing through an intronic silencer. Abstract Text:

    junlin qiJunlin Qi,shihuang suShihuang Su,william mattoxWilliam Mattox,

    The activation of sex-specific alternative splice sites in the Drosophila melanogaster doublesex and fruitless pre-mRNAs has been well studied and depends on the serine-arginine-rich (SR) splicing factors Tra, Tra2, and Rbp1. Little is known, however, about how SR factors negatively regulate splice sites in other RNAs. Here we examine how Tra2 blocks splicing of the M1 intron from its own transcript. We identify an intronic splicing silencer (ISS) adjacent to the M1 branch point that is sufficient to confer Tra2-dependent repression on another RNA. The ISS was found to function independently of its position within the intron, arguing against the idea that bound repressors function by simply interfering with branch point accessibility to general splicing factors. Conserved subelements of the silencer include five short repeated sequences that are required for Tra2 binding but differ from repeated binding sites found in Tra2-dependent splicing enhancers. The ISS also contains a consensus binding site for Rbp1, and this protein was found to facilitate repression of M1 splicing both in vitro and in Drosophila larvae. In contrast to the cooperative binding of SR proteins observed on the doublesex splicing enhancer, we found that Rbp1 and Tra2 bind to the ISS independently through distinct sequences. Our results suggest that functionally synergistic interactions of these SR factors can cause either splicing activation or repression.

    The doublesex splicing enhancer components Tra2 and Rbp1 also repress splicing through an intronic silencer. Publishing Authors By Initials

    j qiJ Qi,s suS Su,w mattoxW Mattox,

    For similar biochemical phenomena, metabolism, and nutrition: biochemical phenomena: molecular structure: base sequence: regulatory sequences, nucleic acid: silencer elements, transcriptional research abstracts see: biochemical phenomena, metabolism, and nutrition: biochemical phenomena: molecular structure: base sequence: regulatory sequences, nucleic acid: silencer elements, transcriptional research

    PUBMED ID PMID:

    MEDLINE DATE:

    The doublesex splicing enhancer components Tra2 and Rbp1 also repress splicing through an intronic silencer. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Molecular and cellular biology

    VOLUME: 27

    Page Numbers: 699-708

    Journal Abbreviation: Mol. Cell. Biol.

    ISSN: 0270-7306

    DAY: 13

    MONTH: 11

    YEAR: 2006

    The doublesex splicing enhancer components Tra2 and Rbp1 also repress splicing through an intronic silencer. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8109087

    The doublesex splicing enhancer components Tra2 and Rbp1 also repress splicing through an intronic silencer. Keywords Mesh Terms:

    KEYWORDS: Silencer Elements, Transcriptional

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: The doublesex splicing enhancer components Tra2 and Rbp1 also repress splicing through an intronic silencer. Information

    Substance Name: tra2 protein, Drosophila

    Registry Number: 0

    Grant and Affiliation Information for The doublesex splicing enhancer components Tra2 and Rbp1 also repress splicing through an intronic silencer.

    AFFILIATION: Department of Molecular Genetics, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030-4009, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIGMS

    GRANT: R01 GM 070892

    ACRONYM: GM

    MEDLINETA: Mol Cell Biol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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