Genetic interactions between [; PSI; +; ] and nonstop mRNA decay affect phenotypic variation Journal Article uri icon

Overview

abstract

  • ; 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.;

publication date

  • July 19, 2005

has restriction

  • bronze

Date in CU Experts

  • February 20, 2014 11:56 AM

Full Author List

  • Wilson MA; Meaux S; Parker R; van Hoof A

author count

  • 4

Other Profiles

International Standard Serial Number (ISSN)

  • 0027-8424

Electronic International Standard Serial Number (EISSN)

  • 1091-6490

Additional Document Info

start page

  • 10244

end page

  • 10249

volume

  • 102

issue

  • 29