Insulin-like Receptor: The First Step into Drosophila melanogaster's Insulin-signaling Pathway
Date
2014-06-02
Authors
Journal Title
Journal ISSN
Volume Title
Publisher
Abstract
Many details about the mechanisms that regulate homeostasis still remain unknown, and metabolic diseases continue to cause a great deal of human suffering. In order to further our understanding of the mechanisms underlying metabolism, I am studying the insulin-signaling pathway and its associated genes. Similar to the insulin-signaling regulated human liver and its storage of excess glucose, Drosophila melanogaster’s larval fat body stores and provides energy during starvation when the animal is immobilized when undergoing metamorphosis. In addition to sustaining homeostasis throughout starvation, this fat body is also one of the only organs saved from programmed cell death during metamorphosis, which is instead remodeled to equally distribute the nutrients through the developing adult body. During larval fat body remodeling, a continuous sheet of polygonal cells spread throughout the pupa by detaching and breaking apart into individual cells.
The insulin-signaling pathway in D. melanogaster involves not only the storage and subsequent release of energy, but that particular organ also undergoes remodeling, which is beneficial to researchers trying to understand both insulin-related and tissue remodeling issues. Though the basics of the insulin-signaling pathway have long been studied, specific genes and their individual effects remain unclear. In order to further understand this signaling pathway, I am examining the insulin receptor homolog known as the Drosophila insulin-like receptor (dInR or InR). Flies overexpressing the InR gene specifically in the larval fat body were generated and whole animals and fat body obtained at different points after puparium formation (APF), the beginning of metamorphosis, were compared to both a positive and negative control using fluorescence microscopy. Obtained results suggest that the fat body remodeling process may be hindered or delayed in D. melanogaster overexpressing the insulin-like receptor in the larval fat body.
Description
Keywords
Drosophila melanogaster, tissue remodeling, insulin-signaling pathway, Drosophila insulin-like receptor, dInR