Chromosome VIII disomy influences the nonsense suppression efficiency and transition metal tolerance of the yeast <i>Saccharomyces cerevisiae</i>

Zadorsky, S. P.; Sopova, Julia V.; Andreichuk, D. Y.; Startsev, V. A.; Medvedeva, Vera; Инге-Вечтомов, С. Г.

doi:10.1002/yea.3074

Cited by 8 publications

(9 citation statements)

References 43 publications

(51 reference statements)

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“…Apart from 15V-P4, we analyzed genomes of four haploid laboratory strains. 25-25-2V-P3982 (the full name of the strain is 25-25-dU8-132-L28-2V-P3982) [ 23 ] is a laboratory strain of a presumably pure Peterhof origin, while 1B-D1606 [ 15 ], 74-D694 [ 24 ], and 6P-33G-D373 Asp + [ 25 , 26 ] descend from hybrids between Peterhof and S288C-derived strains (further referred to as strains of hybrid origin). The pedigree of strains selected for whole genome sequencing is shown in S1 Fig .…”

Section: Resultsmentioning

confidence: 99%

“…74 and its derivatives have been exploited to study the [ PSI + ] prion [ 24 ], and genomic data for a [ PSI + ] variant of this strain was published earlier [ 30 ]. 6P-33G was particularly interesting because it has been recently shown to be disomic for chromosome VIII [ 26 ] and could therefore serve as a control in copy number variation analysis. 1B and 6P-33G are closely related ( S1 Fig ), which might provide material to study recombination patterns.…”

Section: Resultsmentioning

confidence: 99%

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Genome Sequencing and Comparative Analysis of Saccharomyces cerevisiae Strains of the Peterhof Genetic Collection

et al. 2016

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The Peterhof genetic collection of Saccharomyces cerevisiae strains (PGC) is a large laboratory stock that has accumulated several thousands of strains for over than half a century. It originated independently of other common laboratory stocks from a distillery lineage (race XII). Several PGC strains have been extensively used in certain fields of yeast research but their genomes have not been thoroughly explored yet. Here we employed whole genome sequencing to characterize five selected PGC strains including one of the closest to the progenitor, 15V-P4, and several strains that have been used to study translation termination and prions in yeast (25-25-2V-P3982, 1B-D1606, 74-D694, and 6P-33G-D373). The genetic distance between the PGC progenitor and S288C is comparable to that between two geographically isolated populations. The PGC seems to be closer to two bakery strains than to S288C-related laboratory stocks or European wine strains. In genomes of the PGC strains, we found several loci which are absent from the S288C genome; 15V-P4 harbors a rare combination of the gene cluster characteristic for wine strains and the RTM1 cluster. We closely examined known and previously uncharacterized gene variants of particular strains and were able to establish the molecular basis for known phenotypes including phenylalanine auxotrophy, clumping behavior and galactose utilization. Finally, we made sequencing data and results of the analysis available for the yeast community. Our data widen the knowledge about genetic variation between Saccharomyces cerevisiae strains and can form the basis for planning future work in PGC-related strains and with PGC-derived alleles.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Genome Sequencing and Comparative Analysis of Saccharomyces cerevisiae Strains of the Peterhof Genetic Collection

et al. 2016

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“…In line with functional roles of this protein in translation, overexpression of Sbp1 rescues the defect in nonsense suppression caused by SUP35 mutant (Zadorsky et al 2015). Furthermore, in a study on RNA-binding protein FUS/ TLS-dependent cytotoxicity that causes a subset of familial amyotrophic lateral sclerosis (fALS) using yeast as a model system, overexpression of Sbp1 rescues the toxicity caused by FUS/TLS mutations (Ju et al 2011).…”

Section: Introductionmentioning

confidence: 82%

Sbp1 modulates the translation of Pab1 mRNA in a poly(A)- and RGG-dependent manner

Brandariz-Núñez

Zeng

Lam

et al. 2017

RNA

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RNA-binding protein Sbp1 facilitates the decapping pathway in mRNA metabolism and inhibits global mRNA translation by an unclear mechanism. Here we report molecular interactions responsible for Sbp1-mediated translation inhibition of mRNA encoding the polyadenosine-binding protein (Pab1), an essential translation factor that stimulates mRNA translation and inhibits mRNA decapping in eukaryotic cells. We demonstrate that the two distal RRMs of Sbp1 bind to the poly(A) sequence in the 5 ′ ′ ′ ′ ′ UTR of the Pab1 mRNA specifically and cooperatively while the central RGG domain of the protein interacts directly with Pab1. Furthermore, methylation of arginines in the RGG domain abolishes the protein-protein interaction and the inhibitory effect of Sbp1 on translation initiation of Pab1 mRNA. Based on these results, the underlying mechanism for Sbp1-specific translational regulation is proposed. The functional differences of Sbp1 and RGG repeats alone on transcript-specific translation were observed, and a comparison of the results suggests the importance of remodeling the 5 ′ ′ ′ ′ ′ UTR by RNA-binding proteins in mRNA translation.

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“…Among such candidate genes could be several tRNA genes or the sup45-400 allele , as introduction of wild-type SUP45 to Isp + strains has been shown to mimic the Isp − phenotype [13]. To the extent of our knowledge, this is the second reported case of nonsense suppressor phenotype modulated by aneuploidy, the first being chromosome VIII disomy elevating translation termination efficiency due to SPB1 duplication [16]. …”

Section: Discussionmentioning

confidence: 99%

“…the [ PSI + ] prion [15], or an additional chromosome [16]. Similar to suppressor mutations and prions, presence of an additional chromosome may confer adaptiveness or counter-adaptiveness depending on the conditions tested [17, 18].…”

Section: Introductionmentioning

confidence: 99%

Haploid yeast cells undergo a reversible phenotypic switch associated with chromosome II copy number

2016

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Background SUP35 and SUP45 are essential genes encoding polypeptide chain release factors. However, mutants for these genes may be viable but display pleiotropic phenotypes which include, but are not limited to, nonsense suppressor phenotype due to translation termination defect. [PSI +] prion formation is another Sup35p-associated mechanism leading to nonsense suppression through decreased availability of functional Sup35p. [PSI +] differs from genuine sup35 mutations by the possibility of its elimination and subsequent re-induction. Some suppressor sup35 mutants had also been shown to undergo a reversible phenotypic switch in the opposite direction. This reversible switching had been attributed to a prion termed [ISP +]. However, even though many phenotypic and molecular level features of [ISP +] were revealed, the mechanism behind this phenomenon has not been clearly explained and might be more complex than suggested initially.ResultsHere we took a genomic approach to look into the molecular basis of the difference between the suppressor (Isp−) and non-suppressor (Isp+) phenotypes. We report that the reason for the difference between the Isp+ and the Isp− phenotypes is chromosome II copy number changes and support our finding with showing that these changes are indeed reversible by reproducing the phenotypic switch and tracking karyotypic changes. Finally, we suggest mechanisms that mediate elevation in nonsense suppression efficiency upon amplification of chromosome II and facilitate switching between these states.Conclusions(i) In our experimental system, amplification of chromosome II confers nonsense suppressor phenotype and guanidine hydrochloride resistance at the cost of overall decreased viability in rich medium. (ii) SFP1 might represent a novel regulator of chromosome stability, as SFP1 overexpression elevates frequency of the additional chromosome loss in our system. (iii) Prolonged treatment with guanidine hydrochloride leads to selection of resistant isolates, some of which are disomic for chromosome II.Electronic supplementary materialThe online version of this article (doi:10.1186/s12863-016-0464-4) contains supplementary material, which is available to authorized users.

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Chromosome VIII disomy influences the nonsense suppression efficiency and transition metal tolerance of the yeast Saccharomyces cerevisiae

Cited by 8 publications

References 43 publications

Genome Sequencing and Comparative Analysis of Saccharomyces cerevisiae Strains of the Peterhof Genetic Collection

Genome Sequencing and Comparative Analysis of Saccharomyces cerevisiae Strains of the Peterhof Genetic Collection

Sbp1 modulates the translation of Pab1 mRNA in a poly(A)- and RGG-dependent manner

Haploid yeast cells undergo a reversible phenotypic switch associated with chromosome II copy number

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