Honors Program


Date of this Version

Spring 3-15-2021

Document Type



DeWitt, H. 2021. Mitochondrial Defense Mechanisms and Induction of Genes in Response to Environmental Stressors. Undergraduate Honors Thesis. University of Nebraska-Lincoln.


Copyright Haley DeWitt 2021.


An organism’s ability to respond to their environment, reduce the impact of stressors, and return to a state of homeostasis is critical for its survival. Human interactions with the environment have become more detrimental as technology has advanced with little regard for the impact of novel chemicals on organisms across multiple taxa. It has been hypothesized that direct exposure to pesticides and chronic exposure to seemingly ‘safe’ chemicals can induce genetic changes that may contribute to neurodegenerative diseases in humans. For organismal homeostasis, physiological defense mechanisms can be activated in response to the stressors. A well-characterized approach in mammals is by upregulating Uncoupling Proteins (UCPs) in response to high levels of reactive oxygen species (ROS) produced by chemical exposure. However, the presence of this ROS-mediated defense mechanism remains unknown in insects; which has 5.5 million species (or 40% of total organisms on Earth). Here we address the question, do the presence of environmental stressors induce significant ROS-mediated stress responses in insects and if so is there genetic variation for this response? We addressed this question in the model organism, the fruit fly Drosophila melanogaster, by investigating induction of dUCP gene expression in response to ethanol, a stressor frequently encountered by flies in their environment. The Cap ‘n’ Collar (CNC) transcription factor is upregulated in times of stress and we hypothesized that it may bind antioxidant response elements upstream of the dUCPs. Bioinformatic approaches were used to search for antioxidant response elements that bind the CNC transcription factor in dUCPs and in genes that respond to another important environmental stressor paraquat; which is known to cause neurotoxicity in humans. We found that ethanol decreased rather than induced dUCP gene expression, and that genotypes known to produce high ROS did not express dUCP at higher levels than did control genotypes in response to ethanol. We found that gene sets induced in response to paraquat are enriched for putative antioxidant response elements that bind CNC, but dUCPs were not. Future directions will measure relative expression of dUCPs using paraquat as it is known to induce elevated ROS levels. The findings emphasize the importance in continuing to close these knowledge gaps relating to stress responses in non-mammalian organisms, especially as neurotoxicity contributes to a growing public health concern.