Optogenetic Manipulation of Caenorhabditis elegans Pharyngeal Muscles Inhibit Food Consumption
MetadataShow full item record
Obesity, a complex condition that arises from a host of interwoven environmental, cultural, social, and genetic factors, is associated with many devastating diseases. However, resolving the intricacies of obesity-related genes and molecular mechanisms could be especially promising in addressing genetic predispositions to obesity. In mammals, the signaling molecule neuropeptide Y (NPY) is involved in various processes related to obesity, including fat generation, thermogenesis, moderation of feeding behavior, cardiovascular regulation, and much more. By identifying the phenotype of NPY that benefits an organism’s fitness, we propose that we can discern why certain alleles of the gene arose in the population, leading to a better idea of potential physiological functions to target in obesity treatments. Conveniently, the simple nematode worm C. elegans has a homolog of human NPY receptors which is encoded by the npr-1 gene. This gene, in addition to the C. elegans globin protein gene glb-5, has an effect on both fitness and food consumption via unclear, complex mechanisms and potential pleiotropic effects. Considering the theorized links between fitness and genetic predispositions for obesity, these genes could have direct applications to the study of obesity in humans. Here, we design an optogenetics experimental paradigm which will eventually allow us to explore causative connections between food consumption, lifespan, fitness, and reproduction as a result of differences in npr-1 and glb-5 alleles. Using a 90s on/30s off LED cycle, we are able to restrict food consumption C. elegans. This process will be the first step in providing insight into potential mechanisms salient to energy metabolism, satiety, and genetic predispositions to obesity.