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Genetic interactions between [PSI+] and nonstop mRNA decay affect phenotypic variation.
Marenda A Wilson1, Stacie Meaux, Roy Parker
1Department of Microbiology and Molecular Genetics, University of Texas Health Science Center, 6431 Fannin Street, MSB 1.212, Houston, TX 77030, USA.
Summary
The yeast [PSI+] prion causes phenotypic variation by read-through of stop codons, potentially creating new proteins. Nonstop mRNA decay limits this variation, allowing evolution of beneficial protein extensions.
Area of Science:
- Molecular Biology
- Yeast Genetics
- Prion Biology
Background:
- Yeast strains exhibit reversible [PSI+] and [psi-] states.
- [PSI+] is a prion form of eRF3, a translation termination factor.
- The [PSI+] state induces phenotypic variation through stop codon read-through, but mechanisms are unclear.
Purpose of the Study:
- Investigate the molecular mechanisms behind [PSI+]-induced phenotypic variation.
- Determine the role of mRNA decay pathways in [PSI+]-mediated phenotypic changes.
Main Methods:
- Examined the interaction between [PSI+] and defects in nonstop mRNA decay.
- Assessed the interaction between [PSI+] and nonsense-mediated decay defects.
Main Results:
- Identified a significant interaction between [PSI+] and defects in nonstop mRNA decay.
- Observed minimal interaction between [PSI+] and nonsense-mediated decay defects.
- Showed that [PSI+] phenotypic variation is linked to read-through of normal stop codons, producing extended proteins.
Conclusions:
- [PSI+]-induced phenotypic variation may result from read-through of normal stop codons, generating novel protein variants.
- Nonstop mRNA decay appears to limit [PSI+]-induced phenotypic variation.
- This limitation allows for sampling of 3' UTRs for beneficial protein extensions, driving evolutionary adaptation.