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

Christoph J.O. Kaiser, Stefan W. Grötzinger, Julia M. Eckl, Katharina Papsdorf, Stefan Jordan and Klaus Richter ()
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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

Nature Communications, 2013, vol. 4, issue 1, 1-11

Abstract: 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.

Date: 2013
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DOI: 10.1038/ncomms2575

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