mRNA translation is not a prerequisite for small interfering RNA-mediated mRNA cleavage

Authors

  • George L. Sen,

    1. Department of Molecular Pharmacology, Stanford University School of Medicine, Stanford, CA 94305, USA
    2. Baxter Laboratory in Genetic Pharmacology, Stanford University School of Medicine, 269 Campus Drive, CCSR 4225A, Stanford, CA 94305, USA
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  • Tom S. Wehrman,

    1. Department of Molecular Pharmacology, Stanford University School of Medicine, Stanford, CA 94305, USA
    2. Baxter Laboratory in Genetic Pharmacology, Stanford University School of Medicine, 269 Campus Drive, CCSR 4225A, Stanford, CA 94305, USA
    3. Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305-5175, USA
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  • Helen M. Blau

    Corresponding author
    1. Department of Molecular Pharmacology, Stanford University School of Medicine, Stanford, CA 94305, USA
    2. Baxter Laboratory in Genetic Pharmacology, Stanford University School of Medicine, 269 Campus Drive, CCSR 4225A, Stanford, CA 94305, USA
    3. Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305-5175, USA
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✉ E-mail: hblau@stanford.edu

Abstract

Abstract RNA interference constitutes a major means of eliminating mRNAs, yet how the small interfering RNAs (siRNA) within the RNA-induced silencing complex (RISC) finds its homologous target in the cell remains unknown. An attractive hypothesis is that RNA interference is linked to translation which allows RISC ready access to every translated mRNA. To test whether translation could direct siRNAs to mRNAs, chemical and biological inhibitors of translation and their effects on mRNA cleavage were tested. Our results show that mRNA degradation by siRNAs is not dependent on mRNA translation.

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