Date of Award

5-25-2018

Document Type

Thesis and Dissertation

Degree Name

Master of Science (MS)

Department

School of Biological Sciences

First Advisor

Alysia Vrailas-Mortimer

Second Advisor

Nathan Mortimer

Abstract

Aging is inevitable for all organisms and can be characterized by degeneration of tissue, adecrease in motor function, and impaired stress response. In humans, it is often accompanied by an increased propensity for age related diseases. While all adults experience biological aging (senescence) not all adults experience age-associated disease. Thus, we claim these are not normal prospects of aging. Although the implications of aging are well understood, the molecular underpinnings for these processes remain elusive. As advances in medical science have been successful at prolonging lifespan, they concurrently extend the amount of time spend in diseased states. If we wish to increase the amount of time spend in health, it is important we understand the molecular pathways governing senescence. The research for this thesis project focuses on one of the several theories of aging called the oxidative stress theory. It postulates that aging is due to the accumulation of damage in individual cells by reactive oxygen species (ROS). To investigate this, we use the well-established model organism Drosophila melanogaster. Drosophila have a conserved protein family of p38 mitogen-activated protein kinases (MAPK) that are known to regulate both aging and oxidative stress response. In this study we identify and annotated the functions of p38Kb binding partners at 1 week, 3 weeks, and 5 weeks of age. Additionally, binding partners are identified from flies exposed to the oxidizing chemicals paraquat and hydrogen peroxide. Studying the binding partners of p38Kb can elucidate the role of p38Kb and the pathways it interacts with to mediate aging and the response to oxidative stress.

Comments

Imported from Majewski_ilstu_0092N_11254.pdf

DOI

https://doi.org/10.30707/ETD2020.20210309065832405225.89

Page Count

92

Available for download on Wednesday, March 08, 2023

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