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A network of genes connects polyglutamine toxicity to ploidy control in yeast

Author

Listed:
  • Christoph J.O. Kaiser

    (Technische Universität München)

  • Stefan W. Grötzinger

    (Technische Universität München)

  • Julia M. Eckl

    (Technische Universität München)

  • Katharina Papsdorf

    (Technische Universität München)

  • Stefan Jordan

    (Max von Pettenkofer-Institute and Gene Center, Ludwig-Maximilians-University München)

  • Klaus Richter

    (Technische Universität München)

Abstract

Neurodegeneration is linked to protein aggregation in several human disorders. In Huntington’s disease, the length of a polyglutamine stretch in Huntingtin is correlated to neuronal death. Here we utilize a model based on glutamine stretches of 0, 30 or 56 residues in Saccharomyces cerevisiae to understand how such toxic proteins interfere with cellular physiology. A toxicity-mimicking cytostatic effect is evident from compromised colony formation upon expression of polyglutamines. Interestingly, diploid cells are insensitive to polyglutamines and haploid cells can escape cytostasis by hyperploidization. Using a genome-wide screen for genes required to obtain the cytostatic effect, we identify a network related to the budding process and cellular division. We observe a striking mislocalization of the septins Cdc10 and Shs1 in cells arrested by polyglutamines, suggesting that the septin ring may be a pivotal structure connecting polyglutamine toxicity and ploidy.

Suggested Citation

  • Christoph J.O. Kaiser & Stefan W. Grötzinger & Julia M. Eckl & Katharina Papsdorf & Stefan Jordan & Klaus Richter, 2013. "A network of genes connects polyglutamine toxicity to ploidy control in yeast," Nature Communications, Nature, vol. 4(1), pages 1-11, June.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms2575
    DOI: 10.1038/ncomms2575
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