The [PSI+] yeast prion does not wildly affect proteome composition whereas selective pressure exerted on [PSI+] cells can promote aneuploidy View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-12

AUTHORS

Patrick H. W. Chan, Lisa Lee, Erin Kim, Tony Hui, Nikolay Stoynov, Roy Nassar, Michelle Moksa, Dale M. Cameron, Martin Hirst, Joerg Gsponer, Thibault Mayor

ABSTRACT

The yeast Sup35 protein is a subunit of the translation termination factor, and its conversion to the [PSI +] prion state leads to more translational read-through. Although extensive studies have been done on [PSI +], changes at the proteomic level have not been performed exhaustively. We therefore used a SILAC-based quantitative mass spectrometry approach and identified 4187 proteins from both [psi -] and [PSI +] strains. Surprisingly, there was very little difference between the two proteomes under standard growth conditions. We found however that several [PSI +] strains harbored an additional chromosome, such as chromosome I. Albeit, we found no evidence to support that [PSI +] induces chromosomal instability (CIN). Instead we hypothesized that the selective pressure applied during the establishment of [PSI +]-containing strains could lead to a supernumerary chromosome due to the presence of the ade1-14 selective marker for translational read-through. We therefore verified that there was no prevalence of disomy among newly generated [PSI +] strains in absence of strong selection pressure. We also noticed that low amounts of adenine in media could lead to higher levels of mitochondrial DNA in [PSI +] in ade1-14 cells. Our study has important significance for the establishment and manipulation of yeast strains with the Sup35 prion. More... »

PAGES

8442

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41598-017-07999-8

    DOI

    http://dx.doi.org/10.1038/s41598-017-07999-8

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1091148279

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/28814753


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