Genetic interactions between [PSI+] and nonstop mRNA decay affect phenotypic variation.

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.
Mesh Terms:
Blotting, Northern, Codon, Genotype, Peptide Termination Factors, Phenotype, Prions, Protein Biosynthesis, RNA Stability, Saccharomyces cerevisiae Proteins, Sequence Analysis, DNA, Species Specificity, Yeasts
Proc. Natl. Acad. Sci. U.S.A.
Date: Jul. 19, 2005
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