Haploid Yeast Cells Undergo a Reversible Phenotypic Switch Associated with Chromosome II Copy Number

Overview

Journal BMC Genet

Publisher Biomed Central

Specialties Biotechnology
Molecular Biology

Date 2017 Jan 21

PMID 28105933

Citations 5

Authors

Polina Drozdova

Ludmila Mironova

Galina Zhouravleva

Affiliations

Soon will be listed here.

Abstract

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.

Results: Here 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.

Citing Articles

How Big Is the Yeast Prion Universe?.

Zhouravleva G, Bondarev S, Trubitsina N Int J Mol Sci. 2023; 24(14).

PMID: 37511408 PMC: 10380529. DOI: 10.3390/ijms241411651.

Gene Amplification as a Mechanism of Yeast Adaptation to Nonsense Mutations in Release Factor Genes.

Maksiutenko E, Barbitoff Y, Matveenko A, Moskalenko S, Zhouravleva G Genes (Basel). 2021; 12(12).

PMID: 34946968 PMC: 8701342. DOI: 10.3390/genes12122019.

Chromosome-level genome assembly and structural variant analysis of two laboratory yeast strains from the Peterhof Genetic Collection lineage.

Barbitoff Y, Matveenko A, Matiiv A, Maksiutenko E, Moskalenko S, Drozdova P G3 (Bethesda). 2021; 11(4).

PMID: 33677552 PMC: 8759820. DOI: 10.1093/g3journal/jkab029.

RNA Sequencing Reveals Specific TranscriptomicSignatures Distinguishing Effects of the [⁺] Prion and Deletion in Yeast .

Malovichko Y, Antonets K, Maslova A, Andreeva E, Inge-Vechtomov S, Nizhnikov A Genes (Basel). 2019; 10(3).

PMID: 30871095 PMC: 6471900. DOI: 10.3390/genes10030212.

Computational models in genetics at BGRS\SB-2016: introductory note.

Orlov Y, Baranova A, Markel A BMC Genet. 2017; 17(Suppl 3):155.

PMID: 28105935 PMC: 5249000. DOI: 10.1186/s12863-016-0465-3.

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