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Innate immune and chemically triggered oxidative stress modifies translational fidelity

Author

Listed:
  • Nir Netzer

    (Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA)

  • Jeffrey M. Goodenbour

    (Department of Human Genetics,)

  • Alexandre David

    (Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA)

  • Kimberly A. Dittmar

    (Department of Biochemistry and Molecular Biology,)

  • Richard B. Jones

    (Ben May Institute,)

  • Jeffrey R. Schneider

    (University of Chicago, Chicago, Illinois 60637, USA)

  • David Boone

    (University of Chicago, Chicago, Illinois 60637, USA)

  • Eva M. Eves

    (Ben May Institute,)

  • Marsha R. Rosner

    (Ben May Institute,)

  • James S. Gibbs

    (Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA)

  • Alan Embry

    (Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA)

  • Brian Dolan

    (Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA)

  • Suman Das

    (Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA)

  • Heather D. Hickman

    (Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA)

  • Peter Berglund

    (Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA)

  • Jack R. Bennink

    (Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA)

  • Jonathan W. Yewdell

    (Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA)

  • Tao Pan

    (Department of Biochemistry and Molecular Biology,)

Abstract

Mutation by stealth For cells to function properly the process of translating RNA messengers into proteins needs to be accurate, on the whole. Yet work in HeLa cells now shows that about 1% of methionine residues used in protein synthesis are aminoacylated to 'textbook-incorrect' tRNAs. Surprisingly, the proportion of Met-misacylated tRNAs increases significantly when cells are under stress through viral infection or treatment with viral or bacterial Toll-like receptor ligands. Tests with other amino acids indicate that the phenomenon is limited to Met, and as Met residues are known to protect proteins against damage from reactive oxygen species, one possibility is that Met-misacylation is a natural protective response to cellular stress.

Suggested Citation

  • Nir Netzer & Jeffrey M. Goodenbour & Alexandre David & Kimberly A. Dittmar & Richard B. Jones & Jeffrey R. Schneider & David Boone & Eva M. Eves & Marsha R. Rosner & James S. Gibbs & Alan Embry & Bria, 2009. "Innate immune and chemically triggered oxidative stress modifies translational fidelity," Nature, Nature, vol. 462(7272), pages 522-526, November.
    • Handle: RePEc:nat:nature:v:462:y:2009:i:7272:d:10.1038_nature08576
    DOI: 10.1038/nature08576
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    Cited by:

    1. Clement T Y Chan & Madhu Dyavaiah & Michael S DeMott & Koli Taghizadeh & Peter C Dedon & Thomas J Begley, 2010. "A Quantitative Systems Approach Reveals Dynamic Control of tRNA Modifications during Cellular Stress," PLOS Genetics, Public Library of Science, vol. 6(12), pages 1-9, December.

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