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Methionine sulfoxide reductase deficiency leads to mitochondrial dysfunction in Drosophila melanogaster

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Date Issued:
2011
Summary:
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.
Title: Methionine sulfoxide reductase deficiency leads to mitochondrial dysfunction in Drosophila melanogaster.
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Name(s): Verriotto, Jennifer.
Charles E. Schmidt College of Science
Department of Biological Sciences
Type of Resource: text
Genre: Electronic Thesis Or Dissertation
Date Issued: 2011
Publisher: Florida Atlantic University
Physical Form: electronic
Extent: viii, 48 p. : ill. (some col.)
Language(s): English
Summary: 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.
Identifier: 748263537 (oclc), 3174310 (digitool), FADT3174310 (IID), fau:3678 (fedora)
Note(s): by Jennifer Verriotto.
Thesis (M.S.)--Florida Atlantic University, 2011.
Includes bibliography.
Electronic reproduction. Boca Raton, Fla., 2011. Mode of access: World Wide Web.
Subject(s): Oxidation-reduction reaction
Proteins -- Chemical modification
Genetic regulation
Persistent Link to This Record: http://purl.flvc.org/FAU/3174310
Use and Reproduction: http://rightsstatements.org/vocab/InC/1.0/
Host Institution: FAU