Current Search: Mulholland, Kori. (x)
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Title
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Phenotypic and behavioral effects of methionine sulfoxide reductase deficiency and oxidative stress in Drosophila melanogaster.
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Creator
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Mulholland, Kori., Charles E. Schmidt College of Science, Department of Biological Sciences
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Abstract/Description
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Harman's theory of aging proposes that a buildup of damaging reactive oxygen species (ROS) is one of the primary causes of the deleterious symptoms attributed to aging. Cellular defenses in the form of antioxidants have evolved to combat ROS and reverse damage; one such group is the methionine sulfoxide reductases (Msr), which function to reduce oxidized methionine. MsrA reduces the S enantiomer of methionine sulfoxide, Met-S-(o), while MsrB reduces the R enantiomer, Met-R-(o). The focus of...
Show moreHarman's theory of aging proposes that a buildup of damaging reactive oxygen species (ROS) is one of the primary causes of the deleterious symptoms attributed to aging. Cellular defenses in the form of antioxidants have evolved to combat ROS and reverse damage; one such group is the methionine sulfoxide reductases (Msr), which function to reduce oxidized methionine. MsrA reduces the S enantiomer of methionine sulfoxide, Met-S-(o), while MsrB reduces the R enantiomer, Met-R-(o). The focus of this study was to investigate how the absence of one or both forms of Msr affects locomotion in Drosophila using both traditional genetic mutants and more recently developed RNA interference (RNAi) strains. Results indicate that lack of MsrA does not affect locomotion. However, lack of MsrB drastically reduces rates of locomotion in all age classes. Furthermore, creation of an RNAi line capable of knocking down both MsrA and MsrB in progeny was completed.
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Date Issued
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2013
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PURL
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http://purl.flvc.org/fcla/dt/3362558
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Subject Headings
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Drosophila melanogaster, Genetics, Aging, Molecular aspects, Oxidative stress, Mitochondrial pathology, Cellular signal transduction, Oxidation-reduction reaction, Biochemical markers, Mutation (Biology)
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Format
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Document (PDF)
