Great, Green, Glowing Worms: The Insulin/IGF‐1 Signaling Pathway Regulates C. Elegan Feeding Behavior

Abstract

Type II diabetes mellitus is caused by cellular insulin resistance resulting in increased blood glucose levels. Insulin exerts its actions through a signaling cascade that can be modeled in the Caenorhabditis elegan. The Insulin/IGF‐1 signaling (IIS) pathway found in C. elegans contains the same key genes that are involved in human insulin signaling. These genes include the Daf‐2 gene, encoding for an insulin‐like receptor, the Daf‐16 gene, encoding for transcription factors, and Age‐1 gene, encoding for the phosphatidylinositol 3‐kinase (PI(3)K). When C. elegans sense food in their environment, insulin is released, initiating the IIS pathway, resulting in food uptake via pharyngeal pumping. This study will explore the effects that these specific genes have on feeding behaviors based on how knockout mutations of these genes affect the insulin signaling pathway. To study the pumping rate as in indicator of insulin signaling, we will measure the amount of E. coli in their intestines. The greater the rate of pumping, the higher the concentration of E. coli within the intestines. The worms will be fed GFP‐expressing E. coli so that when placed under a confocal microscope, the E. coli within the intestines will fluoresce. From there the intensity of fluorescence can be analyzed for fluorescence intensity using image analysis software and will be compared between the different mutants. We hypothesize that the Daf‐2 and Age‐1 mutants will show fluorescence indicative of little feeding activity since both of these genes further activate components of the pathway to instigate feeding. However, we hypothesize that the Daf‐16 mutants will show fluorescence similar to that of the wildtype nematodes. This is because Daf‐16 works as a negative inhibitor towards the signaling pathway. This research is significant because it can provide how mutations in homologous genes can contribute to type II diabetes.Support or Funding InformationWe would like to acknowledge the help of Dr. Yadilette Rivera Colon, for her expertise, as well as Emily Burns for her lab assistance. In addition, we would like to thank Eileen Stern for her financial contribution under the Stern Scholarship for Undergraduate Researchers.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.