Mitochondria are ubiquitous and essential organelles for all nucleated cells of higher eukaryotes. They contain their own genome [mtDNA (mitochondrial DNA)], and this autosomally replicating extranuclear DNA encodes a complement of genes whose products are required to couple oxidative phosphorylation. Sequencing of this human mtDNA more than 20 years ago revealed unusual features that included a modified codon usage. Specific deviations from the standard genetic code include recoding of the conventional UGA stop to tryptophan, and, strikingly, the apparent recoding of two arginine triplets (AGA and AGG) to termination signals. This latter reassignment was made because of the absence of cognate mtDNA-encoded tRNAs, and a lack of tRNAs imported from the cytosol. Each of these codons only occurs once and, in both cases, at the very end of an open reading frame. The presence of both AGA and AGG is rarely found in other mammals, and the molecular mechanism that has driven the change from encoding arginine to dictating a translational stop has posed a challenging conundrum. Mitochondria from the majority of other organisms studied use only UAA and UAG, leaving the intriguing question of why human organelles appear to have added the complication of a further two stop codons, AGA and AGG, or have they? In the present review, we report recent data to show that mammalian mitochondria can utilize a −1 frameshift such that only the standard UAA and UAG stop codons are required to terminate the synthesis of all 13 polypeptides.
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December 2010
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Conference Article|
November 24 2010
Translation termination in human mitochondrial ribosomes
Ricarda Richter;
Ricarda Richter
1Mitochondrial Research Group, Institute for Ageing and Health, Newcastle University Medical School, Framlington Place, Newcastle upon Tyne NE2 4HH, U.K.
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Aleksandra Pajak;
Aleksandra Pajak
1Mitochondrial Research Group, Institute for Ageing and Health, Newcastle University Medical School, Framlington Place, Newcastle upon Tyne NE2 4HH, U.K.
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Sven Dennerlein;
Sven Dennerlein
1Mitochondrial Research Group, Institute for Ageing and Health, Newcastle University Medical School, Framlington Place, Newcastle upon Tyne NE2 4HH, U.K.
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Agata Rozanska;
Agata Rozanska
1Mitochondrial Research Group, Institute for Ageing and Health, Newcastle University Medical School, Framlington Place, Newcastle upon Tyne NE2 4HH, U.K.
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Robert N. Lightowlers;
Robert N. Lightowlers
1Mitochondrial Research Group, Institute for Ageing and Health, Newcastle University Medical School, Framlington Place, Newcastle upon Tyne NE2 4HH, U.K.
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Zofia M.A. Chrzanowska-Lightowlers
Zofia M.A. Chrzanowska-Lightowlers
1
1Mitochondrial Research Group, Institute for Ageing and Health, Newcastle University Medical School, Framlington Place, Newcastle upon Tyne NE2 4HH, U.K.
1To whom correspondence should be addressed (email Z.Chrzanowska-Lightowlers@ncl.ac.uk).
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Publisher: Portland Press Ltd
Received:
April 26 2010
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2010 Biochemical Society
2010
Biochem Soc Trans (2010) 38 (6): 1523–1526.
Article history
Received:
April 26 2010
Citation
Ricarda Richter, Aleksandra Pajak, Sven Dennerlein, Agata Rozanska, Robert N. Lightowlers, Zofia M.A. Chrzanowska-Lightowlers; Translation termination in human mitochondrial ribosomes. Biochem Soc Trans 1 December 2010; 38 (6): 1523–1526. doi: https://doi.org/10.1042/BST0381523
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