Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 102, Issue 29, Pages 10244-10249Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0504557102
Keywords
capacitor; evolution; prion
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Funding
- NIGMS NIH HHS [R37 GM045443] Funding Source: Medline
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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 Tend 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.
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