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Title: Iron and mitochondrial aging.
Creator: Paez, Rafael., Harriet L. Wilkes Honors College
Abstract/Description: Aging is a process characterized by accumulated oxidative damage to DNA, proteins, and lipids,which leads to the gradual degeneration of cellular activity. Mitochondria play a central role in aging because they produce both cellular energy and oxidative stress. As resultof accumulated oxidative damage, mitochondria function decays, which leads to a cellular energy deficit and compromises cellular function. Iron is an essential nutrient reequired by mitodhondria to function optimally. It has...
Show moreAging is a process characterized by accumulated oxidative damage to DNA, proteins, and lipids,which leads to the gradual degeneration of cellular activity. Mitochondria play a central role in aging because they produce both cellular energy and oxidative stress. As resultof accumulated oxidative damage, mitochondria function decays, which leads to a cellular energy deficit and compromises cellular function. Iron is an essential nutrient reequired by mitodhondria to function optimally. It has been proved that iron supplementation increases the lifespan of several yeast strains, including superoxide dismutase mutants. We are interested in finding where the iron is going and what it might be doing that is beneficial to the cell. We have used Saccharomyces cerevisiae as our molecular model of aging. Our results indicate that the extra iron is being transported into the mitochoindria.
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Date Issued: 2012
PURL: http://purl.flvc.org/FAU/3359313
Subject Headings: Oxidation, Physiological, Aging, Molecular aspects, Mitochondrial DNA, Yeast fungi, Research, Methodology, Free radicals (Chemistry), Pathophysiology
Format: Document (PDF)

Title: Creation of an aconitase overexpression strain of Saccharomyces cerevisiae for lifespan analysis.
Creator: Nunes, Steve., Harriet L. Wilkes Honors College
Abstract/Description: In my thesis work, I attempted to construct a plasmid that would allow stable integration of genes into the Saccharomyces cerevisiae yeast genome under the control of the repressible TetO promoter. The yeast ACO1 gene was cloned under the control of the TetO operator and the tTA transactivator. This construct was inserted into yeast cells in order to observe the effects of aconitase overexpression on aging. Unfortunately, the transformed cells appeared incapable of aconitase expression as...
Show moreIn my thesis work, I attempted to construct a plasmid that would allow stable integration of genes into the Saccharomyces cerevisiae yeast genome under the control of the repressible TetO promoter. The yeast ACO1 gene was cloned under the control of the TetO operator and the tTA transactivator. This construct was inserted into yeast cells in order to observe the effects of aconitase overexpression on aging. Unfortunately, the transformed cells appeared incapable of aconitase expression as determined by glutamic acid auxptrophy, a phenotype of aconitase mutants. We have sequenced the pIT1ACO1 plasmid and have found many abnormalities in the promoter region. If the plasmid can be made to function as intended, the resulting yeast strain can be used in the future to determine if aconitase plays an important role in cellular aging.
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Date Issued: 2012
PURL: http://purl.flvc.org/FAU/3359306
Subject Headings: Yeast fungi, Research, Methodology, Microbial genetics, Genetic engineering, Aging, Molecular aspects, Cell metabolism, Mutation (Biology)
Format: Document (PDF)

Title: The effect of mutated aconitase on yeast longevity.
Creator: Kwan, CJ., Harriet L. Wilkes Honors College
Abstract/Description: Aconitase is an important enzyme in the citric Acid Cycle, is needed for maintenance of mitochondrial DNA, is a key regulator of iron in the cell, and is very sensitive to oxidative stress. We have isolatd the yeast ACO1 gene, which codes for aconitase, and randomly mutated it to create a mutant library of cells each expressing a different version of ACO1. We will select for oxidative stress resistant aconitase in S. cerevisiae by subjecting strains to successive rounds of heat shock and...
Show moreAconitase is an important enzyme in the citric Acid Cycle, is needed for maintenance of mitochondrial DNA, is a key regulator of iron in the cell, and is very sensitive to oxidative stress. We have isolatd the yeast ACO1 gene, which codes for aconitase, and randomly mutated it to create a mutant library of cells each expressing a different version of ACO1. We will select for oxidative stress resistant aconitase in S. cerevisiae by subjecting strains to successive rounds of heat shock and competitive growth against other mutants. The "winner" of this competition will then be analyzed for which version of aconitase it is expressing, which may lead to increased longevity.
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Date Issued: 2012
PURL: http://purl.flvc.org/FAU/3359310
Subject Headings: Yeast fungi, Research, Microbial genetics, Aging, Molecular aspects, Mutation (Biology), Cell metabolism
Format: Document (PDF)

Title: Developmental delays in methionine sulfoxide reductase mutants in Drosophila Melanogaster.
Creator: Hausman, William, Binninger, David, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Aging is a biological process that has many detrimental effects due to the accumulation of oxidative damage to key biomolecules due to the action of free radicals. Methionine sulfoxide reductase (Msr) functions to repair oxidative damage to methionine residues. Msr comes in two forms, MsrA and MsrB, each form has been shown to reduce a specific enantiomer of bound and free oxidized methionine. Effects of Msr have yet to be studied in the major developmental stages of Drosophila melanogaster...
Show moreAging is a biological process that has many detrimental effects due to the accumulation of oxidative damage to key biomolecules due to the action of free radicals. Methionine sulfoxide reductase (Msr) functions to repair oxidative damage to methionine residues. Msr comes in two forms, MsrA and MsrB, each form has been shown to reduce a specific enantiomer of bound and free oxidized methionine. Effects of Msr have yet to be studied in the major developmental stages of Drosophila melanogaster despite the enzymes elevated expression during these stages. A developmental timeline was determined for MsrA mutant, MsrB mutant, and double null mutants against a wild type control. Results show that the Msr double mutant is delayed approximately 20 hours in the early/mid third instar stage while each of the single mutants showed no significant difference to the wild type. Data suggests that the reasoning of this phenomenon is due to an issue gaining mass.
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Date Issued: 2014
PURL: http://purl.flvc.org/fau/fd/FA00004200, http://purl.flvc.org/fau/fd/FA00004200
Subject Headings: Aging -- Molecular aspects, Cellular signal transduction, Drosophila melanogaster -- Genetics, Mitochondrial pathology, Mutation (Biology), Oxidative stress
Format: Document (PDF)

Title: Methionine sulfoxide reductase A (MsrA) and aging in the anoxia-tolerant freshwater turtle (Trachemys scripta).
Creator: Bruce, Lynsey Erin., Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: The enzyme Methionine sulfoxide reductase A (MsrA) repairs oxidized proteins, and may act as a scavenger of reactive oxygen species (ROS), making it a potential therapeutic target for age-related neurodegenerative diseases. The anoxia-tolerant turtle offers a unique model to observe the effects of oxidative stress on a system that maintains neuronal function following anoxia and reoxygenation, and that ages without senescence. MsrA is present in both the mitochondria and cytosol, with protein...
Show moreThe enzyme Methionine sulfoxide reductase A (MsrA) repairs oxidized proteins, and may act as a scavenger of reactive oxygen species (ROS), making it a potential therapeutic target for age-related neurodegenerative diseases. The anoxia-tolerant turtle offers a unique model to observe the effects of oxidative stress on a system that maintains neuronal function following anoxia and reoxygenation, and that ages without senescence. MsrA is present in both the mitochondria and cytosol, with protein levels increasing respectively 3- and 4-fold over 4 hours of anoxia, and remaining 2-fold higher than basal upon reoxygenation. MsrA was knocked down in neuronally-enriched cell cultures via RNAi transfection. Propidium iodide staining showed no significant cell death during anoxia, but this increased 7-fold upon reoxygenation, suggesting a role for MsrA in ROS suppression during reperfusion. This is the first report in any system of MsrA transcript and protein levels being regulated by oxygen levels.
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Date Issued: 2010
PURL: http://purl.flvc.org/FAU/2683139
Subject Headings: Oxidation-reduction reaction, Proteins, Chemical modification, Turtles, Physiology, Oxygen, Physiological effect, Aging, Molecular aspects
Format: Document (PDF)

Title: Analysis of the Role of Autophagy in Dauer Formation and Dauer Recovery Regulated by TGF-β Signaling Pathway in Caenorhabditis elegans.
Creator: Ritter, Portia, Jia, Kailiang, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Caenorhabditis elegans optionally enter into a dauer diapause phase that results in a prolonged life in a semi-dormant state. Entry into and recovery from dauer diapause includes many physical changes in body structure, physiology, and gene expression. Entry into dauer diapause is regulated by several signaling pathways including transforming growth factor (TGF-β). Autophagy plays an important role in dauer formation and recover. During dauer transformation autophagy is up-regulated and may...
Show moreCaenorhabditis elegans optionally enter into a dauer diapause phase that results in a prolonged life in a semi-dormant state. Entry into and recovery from dauer diapause includes many physical changes in body structure, physiology, and gene expression. Entry into dauer diapause is regulated by several signaling pathways including transforming growth factor (TGF-β). Autophagy plays an important role in dauer formation and recover. During dauer transformation autophagy is up-regulated and may play a role in remodeling the molecular structure for long term survival during dauer diapause. This research helps determine the role of autophagy in dauer development and recovery mediated through the TGF-β signaling pathway. This research also determines in which tissue autophagy is necessary for dauer formation and recovery through TGF-β signaling. This research is shedding light on the function of autophagy in the TGF-β signaling pathway, both processes of which have been linked to tumorigenesis, heart disease and cancer.
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Date Issued: 2017
PURL: http://purl.flvc.org/fau/fd/FA00004921, http://purl.flvc.org/fau/fd/FA00004921
Subject Headings: Aging--Molecular aspects., Aging--Physiological aspects., Caenorhabditis elegans--Molecular genetics., Autophagic vacuoles., Gene expression., Apoptosis., Cellular signal transduction., DNA-binding proteins., Transforming growth factors-beta--Receptors.
Format: Document (PDF)

Title: Molecular and phenotypic characterization of MsrA MsrB mutants of Drosophila melanogaster.
Creator: Robbins, Kelli., Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Aging is a multifactoral biological process of progressive and deleterious changes partially attributed to a build up of oxidatively damaged biomolecules resulting from attacks by free radicals. Methionine sulfoxide reductases (Msrs) are enzymes that repair oxidized methionine (Met) residues found in proteins. Oxidized Met produces two enantiomers, Met-S-(o) and Met-R-(o), reduced by MsrA and MsrB respectively. Unlike other model organisms, our MsrA null fly mutant did not display increased...
Show moreAging is a multifactoral biological process of progressive and deleterious changes partially attributed to a build up of oxidatively damaged biomolecules resulting from attacks by free radicals. Methionine sulfoxide reductases (Msrs) are enzymes that repair oxidized methionine (Met) residues found in proteins. Oxidized Met produces two enantiomers, Met-S-(o) and Met-R-(o), reduced by MsrA and MsrB respectively. Unlike other model organisms, our MsrA null fly mutant did not display increased sensitivity to oxidative stress or shortened lifespan, suggesting that in Drosophila, having either a functional copy of either Msr is sufficient. Here, two Msr mutant types were phenotypically assayed against isogenic controls. Results suggest that only the loss of both MsrA and MsrB produces increased sensitivity to oxidative stress and shortened lifespan, while locomotor defects became more severe with the full Msr knockout fly.
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Date Issued: 2009
PURL: http://purl.flvc.org/FAU/359920
Subject Headings: Genetic regulation, Oxidation-reduction reaction, Proteins, Chemical modification, Aging, Molecular aspects, Mutation (Biology), Cell metabolism, Mitochondrial DNA
Format: Document (PDF)

Title: Role of methionine sulfoxide reductase in thermal-induced spreading depression coma in Drosophila melanogaster.
Creator: Schey, Karin., Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Drosophila melanogaster encounter periods of increased temperature or decreased oxygen in its native environment. One consequence of these environmental stresses is increased production of reactive oxygen species that damage major molecules within cells. Another consequence is that flies fall into a protective coma where biological functions are minimized to conserve energy expenditures. This biological phenomenon is called spreading depression. The overarching aim of this project is to...
Show moreDrosophila melanogaster encounter periods of increased temperature or decreased oxygen in its native environment. One consequence of these environmental stresses is increased production of reactive oxygen species that damage major molecules within cells. Another consequence is that flies fall into a protective coma where biological functions are minimized to conserve energy expenditures. This biological phenomenon is called spreading depression. The overarching aim of this project is to determine if methionine sulfoxide reductases affect entrance or exit from the protective coma induced by acute thermal stress. The data revealed that complete deficiency of Msr in young flies causes a faster induction of the coma. In both young and old flies, Msr does not affect average recovery time but does affect the pattern of recovery from coma. Entrance into the coma is age dependent with young flies maintaining activity longer than before entering into the coma as compared to old flies.
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Date Issued: 2012
PURL: http://purl.flvc.org/FAU/3355873
Subject Headings: Cellular signal transduction, Proteins, Chemical modification, Spreading cortical depression, Oxidation-reduction reaction, Aging, Molecular aspects, Mutation (Biology)
Format: Document (PDF)

Title: Methionine sulfoxide reductase (MSR) modulates lifespan andLocomotion in drosophila melanogaster.
Creator: Bruce, Lindsay, Binninger, David, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: Oxidative stress is considered a major factor in the etiology of age related diseases and the aging process itself. Organisms have developed mechanisms to protect against oxidative damage resulting from increased production of reactive oxygen species during aging. One of the major antioxidant systems is the methionine sulfoxide reductase (Msr) enzyme family. The two major Msr enzymes, MsrA and MsrB, can stereospecifically reduce the S and R epimers, respectively, of methionine sulfoxide in...
Show moreOxidative stress is considered a major factor in the etiology of age related diseases and the aging process itself. Organisms have developed mechanisms to protect against oxidative damage resulting from increased production of reactive oxygen species during aging. One of the major antioxidant systems is the methionine sulfoxide reductase (Msr) enzyme family. The two major Msr enzymes, MsrA and MsrB, can stereospecifically reduce the S and R epimers, respectively, of methionine sulfoxide in proteins back to methionine. This study, using Drosophila melanogaster, decribes the first animal system lacking both MsrA and MsrB. The loss of either MsrA or MsrB had no effect on lifespan in Drosophila, but loss of MsrB results in a slight decrease in locomotor activity from middle age onward. Double mutants lacking both forms of Msr have a significantly decreased lifespan and decreased locomotor activity at all ages examined. The double Msr mutants had no detectable increase in protein oxidation or decrease in mitochondrial function and were not more sensitive to oxidative stress. These results suggested that other cellular antioxidant systems were protecting the flies against oxidative damage and the decreased life span observed in the double knockouts was not due to widespread oxidative damage. However, one cannot exclude limited oxidative damage to a specific locus or cell type. In this regard, it was observed that older animals, lacking both MsrA and MsrB, have significantly reduced levels of dopamine, suggesting there might be oxidative damage to the dopaminergic neurons. Preliminary results also suggest that the ratio of F to G actin is skewed towards G actin in all mutants. The present results could have relevance to the loss of dopaminergic neurons in Parkinson’s disease.
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Date Issued: 2015
PURL: http://purl.flvc.org/fau/fd/FA00004431, http://purl.flvc.org/fau/fd/FA00004431
Subject Headings: Aging -- Molecular aspects, Cellular signal transduction, Drosophila melanogaster -- Genetics, Mitochondrial pathology, Mutation (Biology), Oxidative stress, Proteins -- Chemical modification
Format: Document (PDF)

Title: Autophagy gene atg-18 regulates C. elegans lifespan cell nonautonomously by neuropeptide signaling.
Creator: Minnerly, Justin, Jia, Kailiang, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: In the round worm C. elegans, it has recently been shown that autophagy, a highly conserved lysosomal degradation pathway that is present in all eukaryotic cells, is required for maintaining healthspan and for increasing the adult lifespan of worms fed under dietary restriction conditions or with reduced IGF signaling. It is currently unknown how extracellular signals regulate autophagy activity within different tissues during these processes and whether autophagy functions cell-autonomously...
Show moreIn the round worm C. elegans, it has recently been shown that autophagy, a highly conserved lysosomal degradation pathway that is present in all eukaryotic cells, is required for maintaining healthspan and for increasing the adult lifespan of worms fed under dietary restriction conditions or with reduced IGF signaling. It is currently unknown how extracellular signals regulate autophagy activity within different tissues during these processes and whether autophagy functions cell-autonomously or nonautonomously. We have data that for the first time shows autophagy activity in the neurons and intestinal cells plays a major role in regulating adult lifespan and the longevity conferred by altered IGF signaling and dietary restriction, suggesting autophagy can control these phenotypes cell non-autonomously. We hypothesize that autophagy in the neurons and intestinal cells is an essential cellular process regulated by different signaling pathways to control wild type adult lifespan, IGF mediated longevity and dietary restriction induced longevity. Excitingly we also have found that in animals with reduced IGF signaling autophagy can control longevity in only a small subset of neurons alone. Autophagy in either specific individual chemosensory neurons or a small group of them is completely sufficient to control IGF mediated longevity. This work provides novel insight to the function and regulation of autophagy which will help shed light on understanding this essential process in higher organisms, including mammals.
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Date Issued: 2017
PURL: http://purl.flvc.org/fau/fd/FA00004862, http://purl.flvc.org/fau/fd/FA00004862
Subject Headings: Caenorhabditis elegans--Molecular genetics., Aging--Molecular aspects., Life cycles (Biology), Cell death., Gene expression., Autophagic vacuoles., Apoptosis., Eukaryotic cells.
Format: Document (PDF)

Title: Phenotypic and behavioral effects of methionine sulfoxide reductase deficiency and oxidative stress in Drosophila melanogaster.
Creator: Mulholland, Kori., Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: 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: 2013
PURL: http://purl.flvc.org/fcla/dt/3362558
Subject Headings: Drosophila melanogaster, Genetics, Aging, Molecular aspects, Oxidative stress, Mitochondrial pathology, Cellular signal transduction, Oxidation-reduction reaction, Biochemical markers, Mutation (Biology)
Format: Document (PDF)

Title: Reduced Reproductivity and Larval Locomotion in the Absence of Methionine Sulfoxide Reductase in Drosophila.
Creator: Singkornrat, Diana, Binninger, David, Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description: The inevitable aging process can be partially attributed to the accumulation of oxidative damage that results from the action of free radicals. Methionine sulfoxide reductases (Msr) are a class of enzymes that repair oxidized methionine residues. The two known forms of Msr are MsrA and MsrB which reduce the R- and S- enantiomers of methionine sulfoxide, respectively. Our lab has created the first genetic animal model that is fully deficient for any Msr activity. Previously our lab showed that...
Show moreThe inevitable aging process can be partially attributed to the accumulation of oxidative damage that results from the action of free radicals. Methionine sulfoxide reductases (Msr) are a class of enzymes that repair oxidized methionine residues. The two known forms of Msr are MsrA and MsrB which reduce the R- and S- enantiomers of methionine sulfoxide, respectively. Our lab has created the first genetic animal model that is fully deficient for any Msr activity. Previously our lab showed that these animals exhibit a 20 hour delay in development of the third instar larvae (unpublished data). My studies have further shown that the prolonged third-instar stage is due to a reduced growth rate associated with slower food intake and a markedly slower motility. These Msr-deficient animals also exhibit decreased egg-laying that can be attributed to a lack of female receptivity to mating.
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Date Issued: 2016
PURL: http://purl.flvc.org/fau/fd/FA00004777, http://purl.flvc.org/fau/fd/FA00004777
Subject Headings: Proteins--Chemical modification., Oxidative stress., Oxidation-reduction reaction., Drosophila melanogaster--Genetics., Mitochondrial pathology., Cellular signal transduction., Mutation (Biology), Aging--Molecular aspects.
Format: Document (PDF)

FAU Theses and Dissertations (9)	+ -
Honors Student Theses (3)	+ -

Mutation (Biology) (8)	+ -
Aging (7)	+ -
Molecular aspects (7)	+ -
Cellular signal transduction (4)	+ -
Oxidation-reduction reaction (4)	+ -

Aging--Molecular aspects. (3)	+ -
Cell metabolism (3)	+ -
Chemical modification (3)	+ -
Mitochondrial pathology (3)	+ -
Oxidative stress (3)	+ -
Proteins (3)	+ -
Research (3)	+ -
Yeast fungi (3)	+ -
Aging -- Molecular aspects (2)	+ -
Apoptosis. (2)	+ -
Autophagic vacuoles. (2)	+ -
Caenorhabditis elegans--Molecular genetics. (2)	+ -
Cellular signal transduction. (2)	+ -
Gene expression. (2)	+ -
Methodology (2)	+ -
Microbial genetics (2)	+ -
Mitochondrial DNA (2)	+ -
Aging--Physiological aspects. (1)	+ -
Biochemical markers (1)	+ -
Cell death. (1)	+ -
DNA-binding proteins. (1)	+ -
Drosophila melanogaster (1)	+ -
Drosophila melanogaster -- Genetics (1)	+ -
Drosophila melanogaster--Genetics. (1)	+ -
Drosophila melanogaster -- Genetics (1)	+ -

Electronic Thesis or Dissertation (9)	+ -
thesis (3)	+ -

Charles E. Schmidt College of Science (9)	+ -
Department of Biological Sciences (9)	+ -
Florida Atlantic University (5)	+ -
Binninger, David (3)	+ -
Harriet L. Wilkes Honors College (3)	+ -

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