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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.

Proceedings of the National Academy of Sciences of the United States of America
|July 9, 2005
PubMed

Insights

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.

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