Genetic interactions between [; <i>PSI</i>; <sup>+</sup>; ] and nonstop mRNA decay affect phenotypic variation | CU Experts

; Yeast strains can reversibly interconvert between [; PSI; +; ] and [; psi; -; ] states. The [; PSI; +; ] state is caused by a prion form of the translation termination factor eRF3. The [; PSI; +; ] state causes read-through at stop codons and can lead to phenotypic variation, although the molecular mechanisms causing those phenotypic changes remain unknown. We identify an interaction between [; PSI; +; ]-induced phenotypic variation and defects in nonstop mRNA decay. Nonstop mRNA decay is triggered when a ribosome reaches the 3′ end of the transcript. In contrast, we observed little interaction between [; PSI; +; ]-induced phenotypic variation and defects in nonsense-mediated decay, which lead to suppression of premature stop codons. These results suggest that at least some of the phenotypic effects of [; PSI; +; ] may be due to read-through of “normal” stop codons, thereby producing extended proteins. Moreover, these observations suggest that nonstop mRNA decay may limit [; PSI; +; ]-induced phenotypic variation. Such a process would allow periodic sampling of the 3′ UTR, which can diverge rapidly, for novel and beneficial protein extensions.;

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