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Suppression of a mitochondrial point mutation in a tRNA gene can cast light on the mechanisms of 3′ end-processing

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Abstract

We used a genetic approach to study the nuclear factors involved in the biogenesis of mitochondrial tRNAs. A point mutation in the mitochondrial tRNAAsp gene of Saccharomyces cerevisiae had previously been shown to result in a temperature-sensitive respiratory-deficient phenotype as a result of the absence of 3′ end-processing of the tRNAAsp. Analysis of mitochondrial revertants has shown that all revertants sequenced have a G-A compensatory change at position 53, which restores the hydrogen-bond with the mutated nucleotide. We then searched for nuclear suppressors to identify the nuclear gene(s) involved in mitochondrial tRNA 3′ end-processing. One such suppressor mutation was further characterized: it restores tRNAAsp maturation and growth at 36°C on glycerol medium in heterozygous diploids, but leads to a defective growth phenotype in haploids.

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Communicated by K. Wolf

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Rinaldi, T., Francisci, S., Zennaro, E. et al. Suppression of a mitochondrial point mutation in a tRNA gene can cast light on the mechanisms of 3′ end-processing. Curr Genet 25, 451–455 (1994). https://doi.org/10.1007/BF00351785

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  • DOI: https://doi.org/10.1007/BF00351785

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