Mentor: Dr. Peter Adhihetty
College of Health and Human Performance
"I applied to the scholars program after having volunteered in Dr. Adhihetty's research lab for a few months. I did so in order to take more of a leadership role and to expand my research experience. Upon being selected for the Scholars program, I hope to learn much more about Exercise Physiology in the research community, and also to gain professional experience through compiling and presenting my data at conferences. My goals for this academic year are to finish my senior year with strong grades in my classes, to submit my research for publication in a reputable journal, and to be able to present my research with Dr. Adhihetty's lab at the annual Experimental Biology Conference in Boston, MA in April."
Applied Physiology & Kinesiology
- Undergraduate Award, Stanley Lecture Series (Spring 2012)
- Dean's List Recipient, College of Health and Human Performance (Spring 2012)
- Dance Marathon at the University of Florida
- Delts Make a Difference
Hobbies and Interests
- Working Out
- Spending Time with Friends
- Tailgating for Gator Football Games
Altered levels of mitochondrial morphology proteins in skeletal muscle of mitochondrial DNA mutator mice
The mitochondrial theory of aging proposes that mitochondrial and thus tissue function decreases with age, specifically in post-mitotic tissues such as brain, heart, and skeletal muscle. Thirty years of research indicates that the primary factor is due to mutations in mitochondrial DNA (mtDNA), and the increased number of Reactive Oxygen Species (ROS), which damage cellular structures, that are formed from such mutations. A Cell’s primary defense to such mtDNA mutations is the Polymerase-Gamma (PolG) enzyme, which “proofreads” mtDNA as it replicates. Thus, an animal, such as mice, containing a deficient version of the PolG enzyme (PolG mutator mice) will consequently incur high mutation rates that lead to mitochondrial dysfunction. The purpose of the present study is to investigate the effect of increased mitochondrial DNA mutations on regulators of skeletal muscle mitochondrial biogenesis and morphology in young (3-6 month) and old (8-15 month) PolG and wild-type mice. We propose that because of the mutations, PolG mutator mice will have an age-dependent decrease in the expressions of certain proteins, most notably in PGC-1α, the “master regulator” protein that governs all other mitochondrial protein processes. We believe that the increased mitochondrial DNA mutations of the PolG mice will have negative consequences on oxidative metabolism by producing malfunctioning proteins (or failing to produce any at all) of the electron transport chain. This, in turn will cause an increase in ROS of the muscle cells leading to apoptosis and the accelerated aging phenotype. This would suggest that the expressions of various proteins and the overall function and efficiency of the mitochondria paly a crucial role in the aging process. Theoretically, if one were to eliminate all mtDNA mutations and increase the efficiency of mitochondrial proteins, the aging process would be slowed down.