ArticleBMC molecular biology2007
Inactivation of NMD increases viability of sup45 nonsense mutants in Saccharomyces cerevisiae.
Article in BMC molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- High throughput screening of eukaryotic release factor 1 variants to enhance noncanonical amino acid incorporation.bioRxiv : the preprint server for biology · 2025Article
- APOBEC3B cytidine deaminase targets the non-transcribed strand of tRNA genes in yeast.DNA repair · 2017Article
- Haploid yeast cells undergo a reversible phenotypic switch associated with chromosome II copy number.BMC genetics · 2016Article
- Genome Sequencing and Comparative Analysis of Saccharomyces cerevisiae Strains of the Peterhof Genetic Collection.PloS one · 2016Article
- Review
- Regulation of release factor expression using a translational negative feedback loop: a systems analysis.RNA (New York, N.Y.) · 2012Article
- Autoregulatory systems controlling translation factor expression: thermostat-like control of translational accuracy.RNA (New York, N.Y.) · 2010Review
- 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
- Mutation at tyrosine in AMLRY (GILRY like) motif of yeast eRF1 on nonsense codons suppression and binding affinity to eRF3.International journal of biological sciences · 2008Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe nonsense-mediated mRNA decay (NMD) pathway promotes the rapid degradation of mRNAs containing premature termination codons (PTCs). In yeast Saccharomyces cerevisiae, the activity of the NMD pathway depends on the recognition of the PTC by the translational machinery. Translation termination factors eRF1 (Sup45) and eRF3 (Sup35) participate not only in the last step of protein synthesis but also in mRNA degradation and translation initiation via interaction with such proteins as Pab1, Upf1, Upf2 and Upf3.
resultsIn this work we have used previously isolated sup45 mutants of S. cerevisiae to characterize degradation of aberrant mRNA in conditions when translation termination is impaired. We have sequenced his7-1, lys9-A21 and trp1-289 alleles which are frequently used for analysis of nonsense suppression. We have established that sup45 nonsense and missense mutations lead to accumulation of his7-1 mRNA and CYH2 pre-mRNA. Remarkably, deletion of the UPF1 gene suppresses some sup45 phenotypes. In particular, sup45-n upf1Delta double mutants were less temperature sensitive, and more resistant to paromomycin than sup45 single mutants. In addition, deletion of either UPF2 or UPF3 restored viability of sup45-n double mutants.
conclusionThis is the first demonstration that sup45 mutations do not only change translation fidelity but also acts by causing a change in mRNA stability.
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