ArticleNature communications2013
A network of genes connects polyglutamine toxicity to ploidy control in yeast.
Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Scp160 deletion suppresses TDP-43 aggregation and toxicity inMicrobial cell (Graz, Austria) · 2026Article
- Modifier pathways in polyglutamine (PolyQ) diseases: from genetic screens to drug targets.Cellular and molecular life sciences : CMLS · 2022Review
- Application of yeast to studying amyloid and prion diseases.Advances in genetics · 2020Review
- Yeast Models for the Study of Amyloid-Associated Disorders and Development of Future Therapy.Frontiers in molecular biosciences · 2019Review
- Natural Genetic Variation in Yeast Reveals That NEDD4 Is a Conserved Modifier of Mutant Polyglutamine Aggregation.G3 (Bethesda, Md.) · 2018Article
- Studying Huntington's Disease in Yeast: From Mechanisms to Pharmacological Approaches.Frontiers in molecular neuroscience · 2018Review
- Transient protein-protein interactions perturbeLife · 2016Article
- Multiple discrete soluble aggregates influence polyglutamine toxicity in a Huntington's disease model system.Scientific reports · 2016Article
- Quantitative nature of overexpression experiments.Molecular biology of the cell · 2015Article
- Polyglutamine toxicity in yeast induces metabolic alterations and mitochondrial defects.BMC genomics · 2015Article
- Effect of domestication on the spread of the [PIN+] prion in Saccharomyces cerevisiae.Genetics · 2014Article
- Functional toxicology: tools to advance the future of toxicity testing.Frontiers in genetics · 2014Review
- Defining the limits: Protein aggregation and toxicity in vivo.Critical reviews in biochemistry and molecular biologyReview
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.