Abstract

Genetic data presented in Bell et al. (1977) demonstrated that a mutation in Saccharomyces cerevisiae (designated mia) is responsible for the production of mutant isoaccepting tRNA molecules for some tRNA species. Besides extending this phenotype to other tRNAs, we have shown that mutant isoacceptors are produced at the expense of the normal levels of wild type tRNA and that the presence of mutant isoacceptors has no adverse effects on strains harbouring the mutation. The observation that mia strains have mutant isoacceptors as the predominant tRNA species under certain growth conditions suggests that mutant isoacceptors are biologically active molecules. Pulse-label and chase experiments indicate that mutant isoacceptors are slowly converted to wild type tRNA molecules in vivo, suggesting that they could be precursor molecules. This is consistent with the hypothesis that mia is defective in a modification process in the maturation of tRNA molecules. Analysis of a double mutant that produces mia isoacceptors which also lack N(2)-dimethylguanine shows that some of the modifications to tRNA molecules need not follow a specific sequence.

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