ArticleProceedings of the National Academy of Sciences of the United States of America2005
Genetic interactions between [PSI+] and nonstop mRNA decay affect phenotypic variation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed.
- Detection and Degradation of Stalled Nascent Chains via Ribosome-Associated Quality Control.Annual review of biochemistry · 2020Review
- Quality controls induced by aberrant translation.Nucleic acids research · 2020Review
- Cdc48-associated complex bound to 60S particles is required for the clearance of aberrant translation products.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Ribosome-associated complex and Ssb are required for translational repression induced by polylysine segments within nascent chains.Molecular and cellular biology · 2012Article
- Article
- RNA degradation in Saccharomyces cerevisae.Genetics · 2012Review
- Mechanism of activation of methyltransferases involved in translation by the Trm112 'hub' protein.Nucleic acids research · 2011Article
- Article
- The prion hypothesis: from biological anomaly to basic regulatory mechanism.Nature reviews. Molecular cell biology · 2010Review
- Prions, protein homeostasis, and phenotypic diversity.Trends in cell biology · 2010Article
- Prion dynamics and the quest for the genetic determinant in protein-only inheritance.Current opinion in microbiology · 2009Review
- Robustness: mechanisms and consequences.Trends in genetics : TIG · 2009Review
- Complex adaptations can drive the evolution of the capacitor [PSI], even with realistic rates of yeast sex.PLoS genetics · 2009Article
- Mutants of the Paf1 complex alter phenotypic expression of the yeast prion [PSI+].Molecular biology of the cell · 2009Article
- Evolution of nonstop, no-go and nonsense-mediated mRNA decay and their termination factor-derived components.BMC evolutionary biology · 2008Article
- Inactivation of NMD increases viability of sup45 nonsense mutants in Saccharomyces cerevisiae.BMC molecular biology · 2007Article
- Translation of nonSTOP mRNA is repressed post-initiation in mammalian cells.The EMBO journal · 2007Article
- The conversion of 3' UTRs into coding regions.Molecular biology and evolution · 2007Article
- A genetic code alteration generates a proteome of high diversity in the human pathogen Candida albicans.Genome biology · 2007Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.