Innate immune and chemically triggered oxidative stress modifies translational fidelity

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, Brian Dolan, Suman Das, Heather D. Hickman, Peter Berglund, Jack R. Bennink, Jonathan W. Yewdell () and Tao Pan ()
Additional contact information
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,

Nature, 2009, vol. 462, issue 7272, 522-526

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.

Date: 2009
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DOI: 10.1038/nature08576

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