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.
Wilson
Marenda A
MA
Department of Microbiology and Molecular Genetics, University of Texas Health Science Center, 6431 Fannin Street, MSB 1.212, Houston, TX 77030, USA.
Meaux
Stacie
S
Parker
Roy
R
van Hoof
Ambro
A
D015152:Blotting, Northern; D003062:Codon / Q000235:genetics; D005838:Genotype; D010454:Peptide Termination Factors / Q000235:genetics; D010641:Phenotype; D011328:Prions / Q000235:genetics*; D014176:Protein Biosynthesis / Q000235:genetics*; D020871:RNA Stability / Q000235:genetics*; D029701:Saccharomyces cerevisiae Proteins / Q000235:genetics*; D017422:Sequence Analysis, DNA; D013045:Species Specificity; D015003:Yeasts
D003062:Codon; D010454:Peptide Termination Factors; D011328:Prions; C068068:SUP35 protein, S cerevisiae; D029701:Saccharomyces cerevisiae Proteins; C087971:peptide-chain-release factor 3