ArticlePrion
Prion-dependent lethality of sup45 mutants in Saccharomyces cerevisiae.
Article in Prion. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- Prion-Dependent Lethality ofInternational journal of molecular sciences · 2025Article
- Nonsense Mutations in the YeastInternational journal of molecular sciences · 2020Article
- The Pub1 and Upf1 Proteins Act in Concert to Protect Yeast from Toxicity of the [PSI⁺] Prion.International journal of molecular sciences · 2018Article
- Prions in yeast.Genetics · 2012Review
- Amyloid-mediated sequestration of essential proteins contributes to mutant huntingtin toxicity in yeast.PloS one · 2012Article
- The paradox of viable sup45 STOP mutations: a necessary equilibrium between translational readthrough, activity and stability of the protein.Molecular genetics and genomics : MGG · 2009Article
- The role of translation termination factor eRF1 in the regulation of pseudohyphal growth in Saccharomyces cerevisiae cells.Doklady. Biochemistry and biophysicsArticle
- Identification of genes influencing synthetic lethality of genetic and epigenetic alterations in translation termination factors in yeast.Doklady. Biochemistry and biophysicsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In yeast Saccharomyces cerevisiae translation termination factors eRF1 (Sup45) and eRF3 (Sup35) are encoded by the essential genes SUP45 and SUP35 respectively. Heritable aggregation of Sup35 results in formation of the yeast prion [PSI(+)]. It is known that combination of [PSI(+)] with some mutant alleles of the SUP35 or SUP45 genes in one and the same haploid yeast cell causes synthetic lethality. In this study, we perform detailed analysis of synthetic lethality between various sup45 nonsense and missense mutations on one hand, and different variants of [PSI(+)] on the other hand. Synthetic lethality with sup45 mutations was detected for [PSI(+)] variants of different stringencies. Moreover, we demonstrate for the first time that in some combinations, synthetic lethality is dominant and occurs at the postzygotic stage after only a few cell divisions. The tRNA suppressor SUQ5 counteracts the prion-dependent lethality of the nonsense alleles but not of the missense alleles of SUP45, indicating that the lethal effect is due to the depletion of Sup45. Synthetic lethality is also suppressed in the presence of the C-proximal fragment of Sup35 (Sup35C) that lacks the prion domain and cannot be included into the prion aggregates. Remarkably, the production of Sup35C in a sup45 mutant strain is also accompanied by an increase in the Sup45 levels, suggesting that translationally active Sup35 up-regulates Sup45 or protects it from degradation.
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.