ArticleScientific reports2017
Differential effects of soluble and aggregating polyQ proteins on cytotoxicity and type-1 myosin-dependent endocytosis in yeast.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- GFP-free live neuron quantitative imaging reveals compartmentalization and growth dynamics of polyQ aggregates.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- eIF5A controls mitoprotein import by relieving ribosome stalling at TIM50 translocase mRNA.The Journal of cell biology · 2024Article
- The yeast guanine nucleotide exchange factor Sec7 is a bottleneck in spatial protein quality control and detoxifies neurological disease proteins.Scientific reports · 2023Article
- The GET pathway is a major bottleneck for maintaining proteostasis in Saccharomyces cerevisiae.Scientific reports · 2023Article
- FMN reduces Amyloid-β toxicity in yeast by regulating redox status and cellular metabolism.Nature communications · 2020Article
- Studying Spatial Protein Quality Control, Proteopathies, and Aging Using Different Model Misfolding Proteins inFrontiers in molecular neuroscience · 2018Review
- Studying Huntington's Disease in Yeast: From Mechanisms to Pharmacological Approaches.Frontiers in molecular neuroscience · 2018Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease develops when the polyglutamine (polyQ) repeat in the Huntingtin (Htt) protein is expanded to over 35 glutamines rendering it aggregation-prone. Here, using Htt exon-1 as a polyQ model protein in a genome-wide screen in yeast, we show that the normal and soluble Htt exon-1 is toxic in cells with defects in type-1 myosin-dependent endocytosis. The toxicity of Htt is linked to physical interactions with type-1 myosins, which occur via the Htt proline-rich region, leading to a reduction in actin patch polarization and clathrin-dependent endocytosis. An expansion of the polyQ stretch from 25 to 103 glutamines, which causes Htt aggregation, alleviated Htt toxicity in cells lacking Myo5 or other components involved in early endocytosis. The data suggest that the proline-rich stretch of Htt interacts with type-1 myosin/clathrin-dependent processes and demonstrate that a reduction in the activity of such processes may result in a positive selection for polyQ expansions.
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Registered trials
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