ArticlePloS one2017
A new Caenorhabditis elegans model of human huntingtin 513 aggregation and toxicity in body wall muscles.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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30 citing papers in PubMed, 48 citations in OpenAlex.
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- Effects of Vitamin C Supplementation on Tetrabenazine Treatment in a Caenorhabditis elegans Huntington's Disease Model.microPublication biology · 2026Article
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- Lipid Oxidation at the Crossroads: Oxidative Stress and Neurodegeneration Explored inAntioxidants (Basel, Switzerland) · 2025Review
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- Hetero-oligomerization of TDP-43 carboxy-terminal fragments with cellular proteins contributes to proteotoxicity.Communications biology · 2024Article
- Olfactory dysfunction as an early pathogenic indicator inFrontiers in aging neuroscience · 2024Article
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- Towards Understanding Neurodegenerative Diseases: Insights fromInternational journal of molecular sciences · 2023Review
- Fast detection of slender bodies in high density microscopy data.Communications biology · 2023Article
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- Exploiting flow cytometry for the unbiased quantification of protein inclusions in Caenorhabditis elegans.Journal of neurochemistry · 2022Article
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- Efficient splicing-based RNA regulators for tetracycline-inducible gene expression in human cell culture and C. elegans.Nucleic acids research · 2021Article
- An apparent core/shell architecture of polyQ aggregates in the aging Caenorhabditis elegans neuron.Protein science : a publication of the Protein Society · 2021Article
- Drug discovery: Insights from the invertebrate Caenorhabditis elegans.Pharmacology research & perspectives · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expanded polyglutamine repeats in different proteins are the known determinants of at least nine progressive neurodegenerative disorders whose symptoms include cognitive and motor impairment that worsen as patients age. One such disorder is Huntington's Disease (HD) that is caused by a polyglutamine expansion in the human huntingtin protein (htt). The polyglutamine expansion destabilizes htt leading to protein misfolding, which in turn triggers neurodegeneration and the disruption of energy metabolism in muscle cells. However, the molecular mechanisms that underlie htt proteotoxicity have been somewhat elusive, and the muscle phenotypes have not been well studied. To generate tools to elucidate the basis for muscle dysfunction, we engineered Caenorhabditis elegans to express a disease-associated 513 amino acid fragment of human htt in body wall muscle cells. We show that this htt fragment aggregates in C. elegans in a polyglutamine length-dependent manner and is toxic. Toxicity manifests as motor impairment and a shortened lifespan. Compared to previous models, the data suggest that the protein context in which a polyglutamine tract is embedded alters aggregation propensity and toxicity, likely by affecting interactions with the muscle cell environment.
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