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.
Department of Microbiology and Molecular Genetics, University of Texas Health Science Center, 6431 Fannin Street, MSB 1.212, Houston, TX 77030, USA.
Marenda A
MA
Wilson
Stacie
S
Meaux
Roy
R
Parker
Ambro
A
van Hoof
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