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BMC Genetics

, 17:152

First Online: 22 December 2016DOI: 10.1186-s12863-016-0464-4

Cite this article as: Drozdova, P., Mironova, L. & Zhouravleva, G. BMC Genet 2016 17Suppl 3: 152. doi:10.1186-s12863-016-0464-4


BackgroundSUP35 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.

Conclusionsi 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.

KeywordsAneuploidy Translation termination Nonsense suppression SUP35 Yeast Chromosome instability AbbreviationsaCGHMicroarray-based comparative genomic hybridization

GuHClGuanidine hydrochloride

PCRPolymerase chain reaction

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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Autor: Polina Drozdova - Ludmila Mironova - Galina Zhouravleva

Fuente: https://link.springer.com/

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