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In humans, infections, disease, inflammation, and other injuries to specific tissues have been shown to cause delays in the onset of puberty. It is known that steroid hormones and insulin play a role in these delays, yet it is not

In humans, infections, disease, inflammation, and other injuries to specific tissues have been shown to cause delays in the onset of puberty. It is known that steroid hormones and insulin play a role in these delays, yet it is not understood what is happening with the immune system during this response. Similar results have been found in the fruit fly, Drosophila melanogaster, in which damage to adult precursor tissues triggers developmental delays. This project addresses the immune component of the injury response in Drosophila. The goal is to identify which immune response genes, if any, show a significant change in expression after injury. The general methodologies used were first inducing injury via a temperature- sensitive expression of cell death genes in wing precursor tissues, then examining changes in gene expression of immune response genes before and after injury using real-time PCR. The results show that injury increases the expression of genes Drs, CecA1, and Def while decreasing expression of Rel, Dpt, PGRP-LE, and Tl. The changes in immune gene expression following injury suggest the possibility of an immune component to the systemic injury response. These results can further be explored by using mutations of the immune genes to examine their direct effects on the systemic injury response. This research can eventually lead to preventative measures to protect against developmental delays due to infections and diseases in humans.
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Details

Title
  • IMMUNE RESPONSE TO TISSUE DAMAGE IN DROSOPHILA MELANOGASTER
Date Created
2014-12
Resource Type
  • Text
  • Machine-readable links