Browse Articles

Impact of daf-25 and daf-11 Mutations on Olfactory Function in C. elegans

Gardner et al. | Feb 02, 2019

Impact of daf-25 and daf-11 Mutations on Olfactory Function in C. elegans

Cilia are little hair-like protrusions on many cells in the human body, including those lining the trachea where they play a role in clearing our respiratory tract of mucous and other irritants. Genetic mutations that impair ciliary function have serious consequences on our well-being making it important to understand how ciliary function is regulated. By using a simple organism, such as the worm C. elegans that use cilia to move, the authors explore the effect of certain genetic mutations on the cilia of the worms by measuring their ability to move towards or away from certain odorants.

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Effect of Natural Compounds Curcumin and Nicotinamide on α-synuclein Accumulation in a C. elegans Model of Parkinson’s Disease

Mehrotra et al. | Jan 29, 2018

Effect of Natural Compounds Curcumin and Nicotinamide on α-synuclein Accumulation in a C. elegans Model of Parkinson’s Disease

Parkinson's disease is a neurodegenerative disorder that affects over 10 million people worldwide. It is caused by destruction of dopamine-producing neurons, which results in severe motor and movement symptoms. In this study, the authors investigated the anti-Parkinsonian effects of two natural compounds curcumin and nicotinamide using C. elegans as a model organism.

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The role of xpa-1 and him-1 in UV protection of Caenorhabditis elegans

Tung et al. | Feb 25, 2022

The role of <em>xpa-1</em> and <em>him-1</em> in UV protection of <em>Caenorhabditis elegans</em>

Caenorhabditis elegans xpa-1 and him-1 are orthologs of human XPA and human SMC1A, respectively. Mutations in the XPA are correlated with Xeroderma pigmentosum, a condition that induces hypersensitivity to ultraviolet (UV) radiation. Alternatively, SMC1A mutations may lead to Cornelia de Lange Syndrome, a multi-organ disorder that makes patients more sensitive to UVinduced DNA damage. Both C. elegans genes have been found to be involved in protection against UV radiation, but their combined effects have not been tested when they are both knocked down. The authors hypothesized that because these genes are involved in separate pathways, the simultaneous knockdown of both of these genes using RNA interference (RNAi) in C. elegans will cause them to become more sensitive to UV radiation than either of them knocked down individually. UV protection was measured via the percent survival of C. elegans post 365 nm and 5.4x10-19 joules of UV radiation. The double xpa-1/him-1 RNAi knockdown showed a significantly reduced percent survival after 15 and 30 minutes of UV radiation relative to wild-type and xpa-1 and him-1 single knockdowns. These measurements were consistent with their hypothesis and demonstrated that xpa-1 and him-1 genes play distinct roles in resistance against UV stress in C. elegans. This result raises the possibility that the xpa-1/him-1 double knockdown could be useful as an animal model for studying the human disease Xeroderma pigmentosum and Cornelia de Lange Syndrome.

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Astragalus membranaceus Root Concentration and Exposure Time: Role in Heat Stress Diminution in C. elegans

Chen et al. | Oct 17, 2018

Astragalus membranaceus Root Concentration and Exposure Time: Role in Heat Stress Diminution in <em>C. elegans</em>

In this study, the authors investigated the biological mechanism underlying the actions of a traditional medicinal plant, Astragalus membranaceus. Using C. elegans as an experimental model, they tested the effects of AM root on heat stress responses. Their results suggest that AM root extract may enhance the activity of endogenous pathways that mediate cellular responses to heat stress.

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Synergistic Effects of Metformin and Captopril on C. elegans

Kadıoğlu et al. | Jul 10, 2018

Synergistic Effects of Metformin and Captopril on <em>C. elegans</em>

Kadıoğlu and Oğuzalp study the synergistic effects of Metformin and Captopril, two commonly prescribed drugs for type 2 diabetes and hypertension, respectively. Using C. elegans nematodes as a model system, the authors find that the nematodes decreased in average body length when exposed to Metformin or Captopril individually, but grew 11% in body length when both drugs were used together. Because C. elegans body size is regulated in part by the TGF-β signaling pathway, the authors suggest that synergistic effects of these two drugs may be modulating TGF-β activity, a previously uncharacterized phenomenon.

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The Effect of Different Fructose Diets on the Lifespan of C. elegans

Chen et al. | May 10, 2020

The Effect of Different Fructose Diets on the Lifespan of <em>C. elegans</em>

High-fructose diets consumed widely in modern societies predisposes to metabolic diseases such as diabetes. Using the worm C. elegans, the authors of this study investigated the effect of fructose on the worm's survival rates. They found that worms fed 15% fructose had a lower life expectancy than those on a fructose-free diet. These results suggest that, like in humans, fructose has a negative effect on worm survival, which makes them an easy, attractive model to study the effects of fructose on health.

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Albuterol extends lifespan of Caenorhabditis elegans

Belkin et al. | Oct 19, 2021

Albuterol extends lifespan of <i>Caenorhabditis elegans</i>

The objective of this experiment is to determine if the medication albuterol has a positive impact on the lifespan of C. elegans. We hypothesize that if albuterol is added to the diet of C. elegans, then the lifespan of C. elegans will increase. Albuterol increased the mean lifespan of C. elegans by 4.31 ± 0.13 days, compared to the control group and increased the outer range of the C. elegans lifespan. The method of which this occurred is still unknown.

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Expression of Anti-Neurodegeneration Genes in Mutant Caenorhabditis elegans Using CRISPR-Cas9 Improves Behavior Associated With Alzheimer’s Disease

Mishra et al. | Sep 14, 2019

Expression of Anti-Neurodegeneration Genes in Mutant <em>Caenorhabditis elegans</em> Using CRISPR-Cas9 Improves Behavior Associated With Alzheimer’s Disease

Alzheimer's disease is one of the leading causes of death in the United States and is characterized by neurodegeneration. Mishra et al. wanted to understand the role of two transport proteins, LRP1 and AQP4, in the neurodegeneration of Alzheimer's disease. They used a model organism for Alzheimer's disease, the nematode C. elegans, and genetic engineering to look at whether they would see a decrease in neurodegeneration if they increased the amount of these two transport proteins. They found that the best improvements were caused by increased expression of both transport proteins, with smaller improvements when just one of the proteins is overly expressed. Their work has important implications for how we understand neurodegeneration in Alzheimer's disease and what we can do to slow or prevent the progression of the disease.

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