The Role of KLF3 in the Pathogenesis of a C. Elegans Parkinson’s Model

Overview

Approximately 60,000 Americans are diagnosed with Parkinson’s disease every year Parkinson’s disease is caused by the death of dopaminergic neurons in the midbrain. Previous work has identified Krüppel-like factor 3 (KLF3) as a regulator of aging and lifespan in C. elegans. Considering that Parkinson’s disease is age-related, KLF3’s ability to increase longevity could also affect the pathogenesis of Parkinson’s disease. Three lines of C. elegans; KLF3 overexpression, KLF3 knockout, and Wildtype were used in a food response assay to determine dopamine neuron signaling. The assay is used because when a worm is placed in a plate with food, it makes less body bends than in a plate without food, and this difference is controlled by dopamine neurons. C. elegans were placed on an agar plate with food and without food, and the frequency of the worm’s sinusoidal movement was counted in a period of 20 seconds. The antiaging effect of KLF3 may affect dopamine neuron health, and the dopamine neuron affects the worm’s response to foods, therefore differences in the food response could be related to KLF3. KLF3 overexpression was expected to result in the highest difference in the food response assay, based on its ability to increase longevity. However, C. elegans with KLF3 overexpression saw the lowest difference in the food-response assay, only having a difference of 0.2 and -0.7 body bends between the Off Food and On Food response. Further studies should be conducted to fully understand the role, if any, of KLF3 on Parkinson’s.