A novel type of + 1 frameshift suppressor: a base substitution in the anticodon stem of a yeast mitochondrial serine-tRNA causes frameshift suppression. |
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| Authors: | A Hü ttenhofer, B Weiss-Brummer, G Dirheimer, R P Martin |
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| Affiliation: | Institut de Biologie Moléculaire et Cellulaire du CNRS, Laboratoire de Biochimie, Strasbourg, France. |
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| Abstract: | ![]()
We have identified a spontaneous mitochondrial mutation, mfs-1 (mitochondrial frameshift suppressor-1), which suppresses a + 1 frameshift mutation localized in the yeast mitochondrial oxi1 gene. The suppressor strain exhibits a single base change (C to U) at position 42 of the mitochondrial serine-tRNA (UCN). To our knowledge, this is the first reported case showing that a mutation in the anticodon stem of a tRNA can cause frameshift suppression. The expression and aminoacylation of the mutant tRNASer(UCN) are not significantly affected. However, the base change at position 42 has two effects: first, residue U27 of the mutant tRNA is not modified to pseudouridine as observed in wild-type tRNASer(UCN). Second, the base change and/or the lack of modification of U27 leads to an alteration in the secondary/tertiary structure of the mutant tRNA. It is possible that there are such structural changes in the anticodon loop that enable the tRNA to read a four base codon, UCCA, thus restoring the wild-type reading frame. |
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