Glucose effects on polyglutamine-induced proteotoxic stress in Caenorhabditis elegans.

Glucose effects on polyglutamine-induced proteotoxic stress in Caenorhabditis elegans.

Publication date: Nov 27, 2019

Alterations in protein folding may lead to aggregation of misfolded proteins, which is strongly correlated with neurotoxicity and cell death. Protein aggregation has been shown as a normal consequence of aging, but it is largely associated with age-related disease, particularly neurodegenerative diseases like Huntington disease (HD). HD is caused by a CAG repeat expansion in the huntingtin gene and serves as a useful model for neurodegeneration due to its strictly genetic origin. Research in the model organism Caenorhabditis elegans suggests that glucose protects against cell stress, including proteotoxicity related to aggregation, despite the well-known, lifespan-shortening effects of glucose. We hypothesized that glucose could be beneficial by alleviating energy deficiency, a well-characterized phenomenon in HD. We used C. elegans expressing polyglutamine repeats to quantify lifespan, motility, reproduction, learning, and activity of succinate dehydrogenase (SDH), with and without glucose, to identify the role of glucose in proteotoxicity and neuroprotection. Our data show poly-Q worms on glucose plates exhibited shorter lifespans, no change in motility, learning, or SDH product formation, but had altered reproductive phenotypes. Notably, worms expressing toxic polyglutamine repeats were unable to learn association of food with a neutral odorant, even early in life.

Landon, G., Whitney, W., Priya, R., and Mindy, F. Glucose effects on polyglutamine-induced proteotoxic stress in Caenorhabditis elegans. 06807. 2019 Biochem Biophys Res Commun.

Concepts Keywords
Aging SDH
C Elegans Caenorhabditis elegans
Caenorhabditis Elegans Neurodegeneration
Energy Huntingtin
Genetic Huntington’s disease
Glucose Senescence
Huntingtin Organ systems
Huntington Branches of biology
Misfolded Proteins Energy deficiency
Motility
Neurodegeneration
Neurodegenerative Diseases
Neuroprotection
Neurotoxicity
Odorant
Phenotypes
Proteotoxic
Proteotoxicity
SDH
Stress
Succinate Dehydrogenase

Semantics

Type Source Name
drug DRUGBANK Dextrose unspecified form
drug DRUGBANK Succinic acid
pathway KEGG Huntington disease
disease MESH Huntington disease
disease MESH neurodegenerative diseases
disease MESH aging
pathway REACTOME Protein folding

Similar

Original Article

Leave a Comment

Your email address will not be published. Required fields are marked *