Decoding accuracy in eRF1 mutants and its correlation with pleiotropic quantitative traits in yeast

Merritt, Gloria H.; Naemi, Wesley R.; Mugnier, Pierre M.; Webb, Helen; Tuite, Mick F.; Haar, Tobias von der

doi:10.1093/nar/gkq338

Cited by 36 publications

(33 citation statements)

References 50 publications

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“…A study by von der Haar and colleagues showed that a V68A mutation caused a bias against stop codons with an adenine in position three, consistent with our data and the assignment of this residue near cavity three (Merritt et al 2010). However, another study reported that this mutation allowed termination to remain similar to wildtype eRF1 in S. cerevisiae cells (Bertram et al 2000).…”

Section: Discussionsupporting

confidence: 92%

Identification of eRF1 residues that play critical and complementary roles in stop codon recognition

Conard

Buckley²,

Dang³

et al. 2012

RNA

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The initiation and elongation stages of translation are directed by codon-anticodon interactions. In contrast, a release factor protein mediates stop codon recognition prior to polypeptide chain release. Previous studies have identified specific regions of eukaryotic release factor one (eRF1) that are important for decoding each stop codon. The cavity model for eukaryotic stop codon recognition suggests that three binding pockets/cavities located on the surface of eRF1's domain one are key elements in stop codon recognition. Thus, the model predicts that amino acid changes in or near these cavities should influence termination in a stop codon-dependent manner. Previous studies have suggested that the TASNIKS and YCF motifs within eRF1 domain one play important roles in stop codon recognition. These motifs are highly conserved in standard code organisms that use UAA, UAG, and UGA as stop codons, but are more divergent in variant code organisms that have reassigned a subset of stop codons to sense codons. In the current study, we separately introduced TASNIKS and YCF motifs from six variant code organisms into eRF1 of Saccharomyces cerevisiae to determine their effect on stop codon recognition in vivo. We also examined the consequences of additional changes at residues located between the TASNIKS and YCF motifs. Overall, our results indicate that changes near cavities two and three frequently mediated significant effects on stop codon selectivity. In particular, changes in the YCF motif, rather than the TASNIKS motif, correlated most consistently with variant code stop codon selectivity.

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Section: Discussionsupporting

confidence: 92%

Identification of eRF1 residues that play critical and complementary roles in stop codon recognition

Conard

Buckley²,

Dang³

et al. 2012

RNA

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“…The quantitative analysis performed here contributes to a more differentiated view of the roles of all of these four factors. Table I), and indeed previous work has indicated that these four proteins have a range of non-translational roles in the cell (Amrani et al, 1997;Valentini et al, 2002;Cole and Scarcelli, 2006;Urakov et al, 2006;Halls et al, 2007;Pittman et al, 2009;Merritt et al, 2010). On this basis, we classify Dbp5, Ded1, Pab1, and Hyp2 as multifunctional translation factors.…”

Section: Control By Additional (Multifunctional) Translation Factorssupporting

confidence: 69%

An in vivo control map for the eukaryotic mRNA translation machinery

Firczuk

Kannambath

Pahle

et al. 2013

Molecular Systems Biology

131

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“…The detailed study of a large collection of sup45 mutants accomplished recently confirms the last point of view [48].…”

Section: Discussionsupporting

confidence: 61%

Influence of UPF genes on severity of SUP45 mutations

Zhouravleva

Gryzina

2012

Mol Biol

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Eukaryotic cells possess a special mechanism for the degradation of mRNAs containing prema ture termination codons (PTCs), referred to as NMD (nonsense mediated mRNA decay). The strength of this pathway depends on the recognition of the PTCs by translational machinery and the interaction of trans lation termination factors eRF1 and eRF3 with Upf1, Upf2 and Upf3 proteins in Sachromyces cerevisiae yeast. Previously, we have shown that the decrease of eRF1 protein amounts in sup45 nonsense mutants leads to the impairment of NMD. Here we show that the deletion of UPF1 or UPF2 genes leads to an increase in the viability of sup45 mutants, while the effect of UPF3 gene deletion is allele specific. Two hybrid data have shown that amino acid residues 1 555 of Upf1 protein interact with eRF1. Any UPF gene deletion leads to allosupression of the adel1 14 mutation without a change in eRF1 content. The Upf1 depletion does not influence the synthetic lethality of sup45 mutations and the [PSI + ] prion. It is possible that the absence of Upf1 (or its activator Upf2) leads to a more effective formation of the translation termination complex and consequently to the increased viability of the cells containing mutant termination factors.

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Decoding accuracy in eRF1 mutants and its correlation with pleiotropic quantitative traits in yeast

Cited by 36 publications

References 50 publications

Identification of eRF1 residues that play critical and complementary roles in stop codon recognition

Identification of eRF1 residues that play critical and complementary roles in stop codon recognition

An in vivo control map for the eukaryotic mRNA translation machinery

Influence of UPF genes on severity of SUP45 mutations

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