Date of Award
2011
Document Type
Thesis
Publication Status
Version of Record
Submission Date
October 2026
Abstract
Mitochondria are a major source of reactive oxygen species and are particularly vulnerable to oxidative stress. Mitochondrial dysfunction, methionine oxidation, and oxidative stress are thought to play a role in both the aging process and several neurodegenerative diseases. Two major classes of methionine sulfoxide reductases, designated MsrA and MsrB are enzymes that function to repair the enatiomers of methionine sulfoxide, met-(o)-S and met-(o)- R, respectively. This study focuses on the effect of Msr deficiencies on mitochondrial function by utilizing mutant alleles of MsrA and MsrB. The data show that loss of only one form of Msr in the mitochondria does not completely impair the function of the mitochondria. However, loss of both Msr proteins within the mitochondria leads to an increased ROS production and a diminished energy output of the mitochondria. These results support the hypothesis that Msr plays a key role in proper mitochondrial function.
Extent
viii, 48 p. : ill. (some col.)
Recommended Citation
Verriotto, Jennifer., "Methionine sulfoxide reductase deficiency leads to mitochondrial dysfunction in Drosophila melanogaster" (2011). Electronic Theses and Dissertations 2010 - 2019. 333.
https://digitalcommons.fau.edu/etd_general_6/333
Identifier
FADT3174310
Comments
by Jennifer Verriotto.|Thesis (M.S.)--Florida Atlantic University, 2011.|Includes bibliography.|Electronic reproduction. Boca Raton, Fla., 2011. Mode of access: World Wide Web.|by Jennifer Verriotto.