subject:(Mitochondria)

University of Georgia

1. McManus, Meagan Joy. The role of mitochondrial dysfunction and oxidative stress in age-dependent neurodegeneration: implications for the use of mitochondria-targeted therapeutics.

Degree: PhD, Pharmacy, 2010, University of Georgia

URL: http://purl.galileo.usg.edu/uga_etd/mcmanus_meagan_j_201012_phd

► The work presented herein illustrates the multifaceted role of mitochondria in neurodegeneration and provides evidence supporting the use of mitochondria-targeted therapeutics in diseases involving oxidative… (more)

▼ The work presented herein illustrates the multifaceted role of mitochondria in neurodegeneration and provides evidence supporting the use of mitochondria-targeted therapeutics in diseases involving oxidative stress and metabolic failure, namely Alzheimer’s disease (AD). The results implicate mitochondria-derived reactive species (RS) as a central mediator of neuronal apoptosis. The data suggest that while JNK activation is involved in many forms of apoptosis, it is not necessary for mitochondrial RS generation, which may explain its limited role in dictating apoptogenic cytochrome c redistrubution in trophic factor-deprived, sympathetic neurons isolated from mice. In order to provide a greater understanding of the relationship between mitochondrial oxidative stress and neuronal demise, mitochondria-targeted antioxidants were tested on in vitro models of neurodegeneration. MitoQ effectively attenuated all critical, mitochondria-dependent events associated with neuronal apoptosis, including superoxide production from the mitochondrial electron transport chain, cytochrome c redistribution, caspase activation, loss of mitochondrial membrane potential, and the ultimate death of the cell. MitoQ also prolonged the commitment to caspase-independent death by protecting the inner mitochondrial membrane (IMM). Conversely, MitoE2 had no effect on caspase-dependent and caspase-independent events leading to neuronal death, which may be due to inadequate accumulation within the IMM and the inability to sufficiently suppress mitochondrial RS. To determine whether the apparent mitochondrial protection conferred by MitoQ was sufficient to prevent the emergence of AD-associated neuropathology in vivo, young, triple-transgenic AD mice were treated with MitoQ for 5 months and the effect on AD progression was analyzed. The results indicate that MitoQ prevented the onset of cognitive decline, oxidative stress, Aβ-accumulation, and activation of apoptotic machinery in female 3xTg-AD mice. These findings provide solid evidence of a role for mitochondrial RS in age dependent neurodegeneration and suggest mitochondria-targeted therapies hold great promise for the treatment of Alzheimer’s disease. Advisors/Committee Members: James Franklin.

Subjects/Keywords: mitochondria

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APA (6^th Edition):

McManus, M. J. (2010). The role of mitochondrial dysfunction and oxidative stress in age-dependent neurodegeneration: implications for the use of mitochondria-targeted therapeutics. (Doctoral Dissertation). University of Georgia. Retrieved from http://purl.galileo.usg.edu/uga_etd/mcmanus_meagan_j_201012_phd

Chicago Manual of Style (16^th Edition):

McManus, Meagan Joy. “The role of mitochondrial dysfunction and oxidative stress in age-dependent neurodegeneration: implications for the use of mitochondria-targeted therapeutics.” 2010. Doctoral Dissertation, University of Georgia. Accessed February 25, 2020. http://purl.galileo.usg.edu/uga_etd/mcmanus_meagan_j_201012_phd.

MLA Handbook (7^th Edition):

McManus, Meagan Joy. “The role of mitochondrial dysfunction and oxidative stress in age-dependent neurodegeneration: implications for the use of mitochondria-targeted therapeutics.” 2010. Web. 25 Feb 2020.

Vancouver:

McManus MJ. The role of mitochondrial dysfunction and oxidative stress in age-dependent neurodegeneration: implications for the use of mitochondria-targeted therapeutics. [Internet] [Doctoral dissertation]. University of Georgia; 2010. [cited 2020 Feb 25]. Available from: http://purl.galileo.usg.edu/uga_etd/mcmanus_meagan_j_201012_phd.

Council of Science Editors:

McManus MJ. The role of mitochondrial dysfunction and oxidative stress in age-dependent neurodegeneration: implications for the use of mitochondria-targeted therapeutics. [Doctoral Dissertation]. University of Georgia; 2010. Available from: http://purl.galileo.usg.edu/uga_etd/mcmanus_meagan_j_201012_phd

University of Alberta

2. Dromparis, Peter R. Mitochondria in Vascular Health and Disease.

Degree: PhD, Department of Medicine, 2013, University of Alberta

URL: https://era.library.ualberta.ca/files/0z708x22n

► Mitochondria generate reactive oxygen species (mROS) and metabolic substrates like alpha-ketogluterate (αKG), in proportion to oxygen, which target extra-mitochondrial effectors to coordinate a cellular response.… (more)

▼ Mitochondria generate reactive oxygen species (mROS) and metabolic substrates like alpha-ketogluterate (αKG), in proportion to oxygen, which target extra-mitochondrial effectors to coordinate a cellular response. For example, acute hypoxia decreases mROS, resulting in pulmonary artery smooth muscle cell (PASMC) contraction and hypoxic pulmonary vasoconstriction. Metabolic suppression can mimic the hypoxic effects, even in normoxia. In cancer, which has suppressed mitochondrial glucose oxidation (GO), reduced mitochondrial-derived signals including mROS and αKG stabilize hypoxia inducible factor 1α (HIF1α), resulting in normoxic activation that contributes to apoptosis resistance and angiogenesis. This metabolic suppression is shared with hyperproliferative and anti-apoptotic cells in the distal pulmonary artery (PA) wall, and is the hallmark of pulmonary arterial hypertension (PHT). Recently, we proposed that endoplasmic reticulum (ER)-stress-induced disruption of an ‘ER-mitochondrial unit’ as a PHT trigger, since the ER provides Ca2+ that is required for many of the key mitochondrial metabolic enzymes like pyruvate dehydrogenase (PDH) and Krebs cycle enzymes like isocitrate dehydrogenase (IDH; produces αKG). We show that like ER-stress, loss of uncoupling protein-2 (UCP2), reduces mitochondrial calcium (Ca2+m) in PASMCs. This suppresses PDH activity, Krebs cycle function and mROS production, activating HIF1α and contributing to apoptosis resistance in vitro. Mice lacking UCP2 spontaneously develop PHT with distal PA remodeling similar to hypoxic wildtype mice (a standard PHT model). This is the first description of UCP2 influencing oxygen sensing and may open a new window for biomarker or therapeutic strategies. We also show targeting ER-stress is a viable therapeutic strategy in PHT. 4-phenylbutyric acid (PBA), a FDA approved chemical chaperone that facilitates protein folding and attenuates ER-stress. PBA prevented and reversed pulmonary vascular remodeling and PHT in chronic hypoxia and monocrotaline rodents. In isolated PASMCs, PBA, and a second chemical chaperone tauroursodeoxycholate maintained Ca2+m, normalizing PDH activity and mROS/αKG, reducing proliferation and inducing apoptosis in hypoxia (an ER-stress inducer). Thus, pathobiology linked with the functional dysregulation between mitochondria and other organelles can be therapeutically targeted. Finally, we show that mitochondrial activation with thiazolidinediones can impair HIF1α signaling in a hindlimb ischemia model, potentially explaining some of the adverse cardiovascular events in some patients with these drugs.

Subjects/Keywords: mitochondria

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APA (6^th Edition):

Dromparis, P. R. (2013). Mitochondria in Vascular Health and Disease. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/0z708x22n

Chicago Manual of Style (16^th Edition):

Dromparis, Peter R. “Mitochondria in Vascular Health and Disease.” 2013. Doctoral Dissertation, University of Alberta. Accessed February 25, 2020. https://era.library.ualberta.ca/files/0z708x22n.

MLA Handbook (7^th Edition):

Dromparis, Peter R. “Mitochondria in Vascular Health and Disease.” 2013. Web. 25 Feb 2020.

Vancouver:

Dromparis PR. Mitochondria in Vascular Health and Disease. [Internet] [Doctoral dissertation]. University of Alberta; 2013. [cited 2020 Feb 25]. Available from: https://era.library.ualberta.ca/files/0z708x22n.

Council of Science Editors:

Dromparis PR. Mitochondria in Vascular Health and Disease. [Doctoral Dissertation]. University of Alberta; 2013. Available from: https://era.library.ualberta.ca/files/0z708x22n

3. Ford, Kara Alexandra. The Role of C-Terminal Src Kinase on Mitochondrial Function.

Degree: Department of Molecular Pharmacology, Physiology and Biotechnology, 2017, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:733329/

► The role of C-Terminal Src Kinase (CSK) in mitochondrial function was evaluated in this thesis. CSK is mainly found in the cytosol and involved in… (more)

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Ford, K. A. (2017). The Role of C-Terminal Src Kinase on Mitochondrial Function. (Thesis). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:733329/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ford, Kara Alexandra. “The Role of C-Terminal Src Kinase on Mitochondrial Function.” 2017. Thesis, Brown University. Accessed February 25, 2020. https://repository.library.brown.edu/studio/item/bdr:733329/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ford, Kara Alexandra. “The Role of C-Terminal Src Kinase on Mitochondrial Function.” 2017. Web. 25 Feb 2020.

Vancouver:

Ford KA. The Role of C-Terminal Src Kinase on Mitochondrial Function. [Internet] [Thesis]. Brown University; 2017. [cited 2020 Feb 25]. Available from: https://repository.library.brown.edu/studio/item/bdr:733329/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ford KA. The Role of C-Terminal Src Kinase on Mitochondrial Function. [Thesis]. Brown University; 2017. Available from: https://repository.library.brown.edu/studio/item/bdr:733329/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Oregon State University

4. Gregg, Charles Thornton. Oxidative phosphorylation and respiratory control in insect mitochondria.

Degree: PhD, Chemistry, 1959, Oregon State University

URL: http://hdl.handle.net/1957/50766

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Gregg, C. T. (1959). Oxidative phosphorylation and respiratory control in insect mitochondria. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/50766

Chicago Manual of Style (16^th Edition):

Gregg, Charles Thornton. “Oxidative phosphorylation and respiratory control in insect mitochondria.” 1959. Doctoral Dissertation, Oregon State University. Accessed February 25, 2020. http://hdl.handle.net/1957/50766.

MLA Handbook (7^th Edition):

Gregg, Charles Thornton. “Oxidative phosphorylation and respiratory control in insect mitochondria.” 1959. Web. 25 Feb 2020.

Vancouver:

Gregg CT. Oxidative phosphorylation and respiratory control in insect mitochondria. [Internet] [Doctoral dissertation]. Oregon State University; 1959. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1957/50766.

Council of Science Editors:

Gregg CT. Oxidative phosphorylation and respiratory control in insect mitochondria. [Doctoral Dissertation]. Oregon State University; 1959. Available from: http://hdl.handle.net/1957/50766

University of Hong Kong

5. Law, Yee-song. Biological roles of atpap2 in the mitochondria.

Degree: PhD, 2015, University of Hong Kong

URL: Law, Y. [劉益松]. (2015). Biological roles of atpap2 in the mitochondria. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5481874 ; http://dx.doi.org/10.5353/th_b5481874 ; http://hdl.handle.net/10722/225944

► Arabidopsis thaliana Purple Acid Phosphatase 2 (AtPAP2) is anchored on the outer membranes of chloroplasts and mitochondria through its C-terminal transmembrane motif. Although the growth… (more)

▼ Arabidopsis thaliana Purple Acid Phosphatase 2 (AtPAP2) is anchored on the outer membranes of chloroplasts and mitochondria through its C-terminal transmembrane motif. Although the growth phenotypes of pap2 T-DNA line appear normal, the Arabidopsis thaliana overexpressing AtPAP2 line (OE7) bolts earlier and produces more seeds. To date, AtPAP2 is the only phosphatase that is known to be anchored on the outer membrane of the mitochondria. The objective of this study was to find out its biological roles in the mitochondria. Cytosolic STY kinases phosphorylate the transit peptides of certain precursor proteins and regulate their import into chloroplasts. In this study, AtPAP2 was showed to interact with seven out of nine multiple organellar RNA editing factor (MORF) family proteins by yeast-two hybrid and bimolecular fluorescence complementation (BiFC) assays. The presequences of several precursor MORF (pMORF) family proteins, which play role in RNA editing in mitochondria and plastids, are phosphorylated by cytosolic STY kinases. STY-phosphorylated pMORF3, but not its non-phosphorylatable mutant (pMORF3-T17/20/35A), can complex with 14-3-3 and HSP70. The import rate of wheat germ lysate (WGL)-synthesized pMORF3-T17/20/35A into mitochondria was much faster than that of WGL-pMORF3 and the import rate of WGL-pMORF3 into mitochondria isolated from the pap2 T-DNA line was slower than that into mitochondria isolated from the wild-type plants. Therefore, STY kinases and AtPAP2 post-translationally regulate the import of the pMORF3 into the mitochondria. Previous studies revealed that the photosynthetic rate of OE7 excess than wild type and its leaves contain higher amounts of ATP, malate, glutamine and asparagine than the wild type at the end of the night (T= 0) and the middle of the day (T= 8). In this study, the iTRAQ quantitative proteomics approach was used to investigate the impact of AtPAP2 overexpression on the mitochondrial proteome. A total of 903 mitochondrial proteins were identified from mitochondria isolated from 20-day-old leaves at T= 0 and T= 8. Proteins differentially expressed between the wild-type and OE7 mitochondria were identified in various pathways, including the respiratory electron chain, tricarboxylic acid (TCA) cycle, RNA editing and mitochondrial protein import components (MPIC). The lower protein abundances of complex I and V subunits at both time points and the lower in-gel activity of complex I at T= 8 in OE7 reflected that the efficiency of the ATP production in OE7 mitochondria may have decreased. At T= 8, OE7 mitochondria contained higher levels of metabolites (glutamine, asparagine and fumarate) and enzymes (mitochondrial isocitrate dehydrogenase 1 and mitochondrial malate dehydrogenase 1) required for nitrogen assimilation; whereas, at T= 0, the high ATP output from chloroplasts at daytime may have suppressed the TCA cycle in the OE line, as the abundances of TCA cycle enzymes between 2-oxoglutarate and malate/OAA in down-regulated when more ATP production is unnecessary. In…

Subjects/Keywords: Mitochondria; Phosphatases

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APA (6^th Edition):

Law, Y. (2015). Biological roles of atpap2 in the mitochondria. (Doctoral Dissertation). University of Hong Kong. Retrieved from Law, Y. [劉益松]. (2015). Biological roles of atpap2 in the mitochondria. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5481874 ; http://dx.doi.org/10.5353/th_b5481874 ; http://hdl.handle.net/10722/225944

Chicago Manual of Style (16^th Edition):

Law, Yee-song. “Biological roles of atpap2 in the mitochondria.” 2015. Doctoral Dissertation, University of Hong Kong. Accessed February 25, 2020. Law, Y. [劉益松]. (2015). Biological roles of atpap2 in the mitochondria. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5481874 ; http://dx.doi.org/10.5353/th_b5481874 ; http://hdl.handle.net/10722/225944.

MLA Handbook (7^th Edition):

Law, Yee-song. “Biological roles of atpap2 in the mitochondria.” 2015. Web. 25 Feb 2020.

Vancouver:

Law Y. Biological roles of atpap2 in the mitochondria. [Internet] [Doctoral dissertation]. University of Hong Kong; 2015. [cited 2020 Feb 25]. Available from: Law, Y. [劉益松]. (2015). Biological roles of atpap2 in the mitochondria. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5481874 ; http://dx.doi.org/10.5353/th_b5481874 ; http://hdl.handle.net/10722/225944.

Council of Science Editors:

Law Y. Biological roles of atpap2 in the mitochondria. [Doctoral Dissertation]. University of Hong Kong; 2015. Available from: Law, Y. [劉益松]. (2015). Biological roles of atpap2 in the mitochondria. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5481874 ; http://dx.doi.org/10.5353/th_b5481874 ; http://hdl.handle.net/10722/225944

Oregon State University

6. Mahlum, Lisa Michelle. Mitochondrial function is a primary variable affecting sperm mobility phenotype in the domestic fowl.

Degree: MS, Animal Science, 2001, Oregon State University

URL: http://hdl.handle.net/1957/32425

► Sperm mobility denotes the net movement of a sperm population. Previous work implicated mitochondrial function as a basis underlying phenotypic variation in this quantitative trait.… (more)

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Mahlum, L. M. (2001). Mitochondrial function is a primary variable affecting sperm mobility phenotype in the domestic fowl. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/32425

Chicago Manual of Style (16^th Edition):

Mahlum, Lisa Michelle. “Mitochondrial function is a primary variable affecting sperm mobility phenotype in the domestic fowl.” 2001. Masters Thesis, Oregon State University. Accessed February 25, 2020. http://hdl.handle.net/1957/32425.

MLA Handbook (7^th Edition):

Mahlum, Lisa Michelle. “Mitochondrial function is a primary variable affecting sperm mobility phenotype in the domestic fowl.” 2001. Web. 25 Feb 2020.

Vancouver:

Mahlum LM. Mitochondrial function is a primary variable affecting sperm mobility phenotype in the domestic fowl. [Internet] [Masters thesis]. Oregon State University; 2001. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1957/32425.

Council of Science Editors:

Mahlum LM. Mitochondrial function is a primary variable affecting sperm mobility phenotype in the domestic fowl. [Masters Thesis]. Oregon State University; 2001. Available from: http://hdl.handle.net/1957/32425

Oregon State University

7. Will, Yvonne. Use of γ-Glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial dysfunction, and cell death.

Degree: PhD, Biochemistry and Biophysics, 1999, Oregon State University

URL: http://hdl.handle.net/1957/32950

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Will, Y. (1999). Use of γ-Glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial dysfunction, and cell death. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/32950

Chicago Manual of Style (16^th Edition):

Will, Yvonne. “Use of γ-Glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial dysfunction, and cell death.” 1999. Doctoral Dissertation, Oregon State University. Accessed February 25, 2020. http://hdl.handle.net/1957/32950.

MLA Handbook (7^th Edition):

Will, Yvonne. “Use of γ-Glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial dysfunction, and cell death.” 1999. Web. 25 Feb 2020.

Vancouver:

Will Y. Use of γ-Glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial dysfunction, and cell death. [Internet] [Doctoral dissertation]. Oregon State University; 1999. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1957/32950.

Council of Science Editors:

Will Y. Use of γ-Glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial dysfunction, and cell death. [Doctoral Dissertation]. Oregon State University; 1999. Available from: http://hdl.handle.net/1957/32950

Oregon State University

8. Savage, Melani K. Status of mitochondrial glutathione and energy levels during cyclosporin A-sensitive permeability transition induced by calcium and inorganic phosphate.

Degree: PhD, Toxicology, 1994, Oregon State University

URL: http://hdl.handle.net/1957/35585

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Savage, M. K. (1994). Status of mitochondrial glutathione and energy levels during cyclosporin A-sensitive permeability transition induced by calcium and inorganic phosphate. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/35585

Chicago Manual of Style (16^th Edition):

Savage, Melani K. “Status of mitochondrial glutathione and energy levels during cyclosporin A-sensitive permeability transition induced by calcium and inorganic phosphate.” 1994. Doctoral Dissertation, Oregon State University. Accessed February 25, 2020. http://hdl.handle.net/1957/35585.

MLA Handbook (7^th Edition):

Savage, Melani K. “Status of mitochondrial glutathione and energy levels during cyclosporin A-sensitive permeability transition induced by calcium and inorganic phosphate.” 1994. Web. 25 Feb 2020.

Vancouver:

Savage MK. Status of mitochondrial glutathione and energy levels during cyclosporin A-sensitive permeability transition induced by calcium and inorganic phosphate. [Internet] [Doctoral dissertation]. Oregon State University; 1994. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1957/35585.

Council of Science Editors:

Savage MK. Status of mitochondrial glutathione and energy levels during cyclosporin A-sensitive permeability transition induced by calcium and inorganic phosphate. [Doctoral Dissertation]. Oregon State University; 1994. Available from: http://hdl.handle.net/1957/35585

Oregon State University

9. Meegungwan, Chongchit. Evidence for an intermediate related to oxidative phosphorylation in mitochondria from blowflies, Phormia regina.

Degree: MS, General Science, 1964, Oregon State University

URL: http://hdl.handle.net/1957/48070

► A large number of experiments were done to detect and identify one or more intermediates involved in coupling ATP synthesis to electron transport. Using mitochondria… (more)

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Meegungwan, C. (1964). Evidence for an intermediate related to oxidative phosphorylation in mitochondria from blowflies, Phormia regina. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/48070

Chicago Manual of Style (16^th Edition):

Meegungwan, Chongchit. “Evidence for an intermediate related to oxidative phosphorylation in mitochondria from blowflies, Phormia regina.” 1964. Masters Thesis, Oregon State University. Accessed February 25, 2020. http://hdl.handle.net/1957/48070.

MLA Handbook (7^th Edition):

Meegungwan, Chongchit. “Evidence for an intermediate related to oxidative phosphorylation in mitochondria from blowflies, Phormia regina.” 1964. Web. 25 Feb 2020.

Vancouver:

Meegungwan C. Evidence for an intermediate related to oxidative phosphorylation in mitochondria from blowflies, Phormia regina. [Internet] [Masters thesis]. Oregon State University; 1964. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1957/48070.

Council of Science Editors:

Meegungwan C. Evidence for an intermediate related to oxidative phosphorylation in mitochondria from blowflies, Phormia regina. [Masters Thesis]. Oregon State University; 1964. Available from: http://hdl.handle.net/1957/48070

Oregon State University

10. Petersen, Thomas Gordon. The purification and characterization of a soluble mitochondrial adenosinetriphosphatase from cabbage, Brassica oleracea.

Degree: MA, Chemistry, 1963, Oregon State University

URL: http://hdl.handle.net/1957/48921

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Petersen, T. G. (1963). The purification and characterization of a soluble mitochondrial adenosinetriphosphatase from cabbage, Brassica oleracea. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/48921

Chicago Manual of Style (16^th Edition):

Petersen, Thomas Gordon. “The purification and characterization of a soluble mitochondrial adenosinetriphosphatase from cabbage, Brassica oleracea.” 1963. Masters Thesis, Oregon State University. Accessed February 25, 2020. http://hdl.handle.net/1957/48921.

MLA Handbook (7^th Edition):

Petersen, Thomas Gordon. “The purification and characterization of a soluble mitochondrial adenosinetriphosphatase from cabbage, Brassica oleracea.” 1963. Web. 25 Feb 2020.

Vancouver:

Petersen TG. The purification and characterization of a soluble mitochondrial adenosinetriphosphatase from cabbage, Brassica oleracea. [Internet] [Masters thesis]. Oregon State University; 1963. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1957/48921.

Council of Science Editors:

Petersen TG. The purification and characterization of a soluble mitochondrial adenosinetriphosphatase from cabbage, Brassica oleracea. [Masters Thesis]. Oregon State University; 1963. Available from: http://hdl.handle.net/1957/48921

Oregon State University

11. Smith, Karin Ann. The relation of a soluble factor to phosphorylation during the oxidation of reduced nicotinamide adenine dinucleotides.

Degree: MA, Chemistry, 1962, Oregon State University

URL: http://hdl.handle.net/1957/48841

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Smith, K. A. (1962). The relation of a soluble factor to phosphorylation during the oxidation of reduced nicotinamide adenine dinucleotides. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/48841

Chicago Manual of Style (16^th Edition):

Smith, Karin Ann. “The relation of a soluble factor to phosphorylation during the oxidation of reduced nicotinamide adenine dinucleotides.” 1962. Masters Thesis, Oregon State University. Accessed February 25, 2020. http://hdl.handle.net/1957/48841.

MLA Handbook (7^th Edition):

Smith, Karin Ann. “The relation of a soluble factor to phosphorylation during the oxidation of reduced nicotinamide adenine dinucleotides.” 1962. Web. 25 Feb 2020.

Vancouver:

Smith KA. The relation of a soluble factor to phosphorylation during the oxidation of reduced nicotinamide adenine dinucleotides. [Internet] [Masters thesis]. Oregon State University; 1962. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1957/48841.

Council of Science Editors:

Smith KA. The relation of a soluble factor to phosphorylation during the oxidation of reduced nicotinamide adenine dinucleotides. [Masters Thesis]. Oregon State University; 1962. Available from: http://hdl.handle.net/1957/48841

Oregon State University

12. Tripp, Martha June. Enzymatic patterns of ionocytes in Oncorhynchus tshawytscha: Ionocytes, Enzymatic patterns.

Degree: MS, General Science, 1967, Oregon State University

URL: http://hdl.handle.net/1957/47315

► Characterization of the enzymatic activity of the ionocyte (mitochondria-rich cell) in the gill epithelium of Oncorhynchus tshawytscha was explored. 1. A method for estimating the… (more)

Subjects/Keywords: Mitochondria

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APA (6^th Edition):

Tripp, M. J. (1967). Enzymatic patterns of ionocytes in Oncorhynchus tshawytscha: Ionocytes, Enzymatic patterns. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/47315

Chicago Manual of Style (16^th Edition):

Tripp, Martha June. “Enzymatic patterns of ionocytes in Oncorhynchus tshawytscha: Ionocytes, Enzymatic patterns.” 1967. Masters Thesis, Oregon State University. Accessed February 25, 2020. http://hdl.handle.net/1957/47315.

MLA Handbook (7^th Edition):

Tripp, Martha June. “Enzymatic patterns of ionocytes in Oncorhynchus tshawytscha: Ionocytes, Enzymatic patterns.” 1967. Web. 25 Feb 2020.

Vancouver:

Tripp MJ. Enzymatic patterns of ionocytes in Oncorhynchus tshawytscha: Ionocytes, Enzymatic patterns. [Internet] [Masters thesis]. Oregon State University; 1967. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1957/47315.

Council of Science Editors:

Tripp MJ. Enzymatic patterns of ionocytes in Oncorhynchus tshawytscha: Ionocytes, Enzymatic patterns. [Masters Thesis]. Oregon State University; 1967. Available from: http://hdl.handle.net/1957/47315

University of Arizona

13. Brown, Daniel Robert. GENETIC VARIATION IN MITOCHONDRIAL RESPIRATORY METABOLISM IN AVIAN AND MAMMALIAN SPECIES.

Degree: 1987, University of Arizona

URL: http://hdl.handle.net/10150/184046

► Comparative studies documented relationships between mitochondrial respiration and phenotype among genetically divergent animals. Broiler chickens' mitochondria ranked higher than layer chickens' for state 3 respiration… (more)

▼ Comparative studies documented relationships between mitochondrial respiration and phenotype among genetically divergent animals. Broiler chickens' mitochondria ranked higher than layer chickens' for state 3 respiration (16.1 ± 0.4 μM O₂/mg protein/min), respiratory control ratio (3.5 ± 0.1) and ADP:O ratio (1.05 ± 0.01 μM ADP/μA O) utilizing succinate. Broilers yielded more (P < .05) mitochondrial protein than did layers (7.8 vs. 6.2 ± 0.2 mg/g hepatic tissue). Within-breed mitochondrial activity had no associations with chicken weight or egg production. C57BL/6J mice mitochondria had higher (P < .05) respiratory control ratios (4.06 vs. 3.78 ± 0.09), and C57BL/6J females higher state 3 respiration rates utilizing succinate (strain by sex interaction P < .01), than A/J or BALB/cJ mice mitochondria. BALB/cJ mitochondria had higher (P < .05) ADP:O ratios utilizing pyruvate than C57BL/6J mitochondria (1.58 vs. 1.46 ± 0.04 μM ADP/μA O). Rapid ATP synthesis rates of C57BL/6J female mice were associated generally with reproductive superiority. Inbred mouse body weight was not associated with mitochondrial respiration. Original data confirmed CB6F₁, but not CAF₁, hybrid mice were heterotic for postweaning growth. Hybridization increased (P < .05) mitochondrial mass, but did not enhance respiration. No association existed between growth heterosis and mitochondrial function in hybrid mice. Unexpected sexual dimorphism in mitochondrial respiration existed across mouse strains. Testosterone administration and orchiectomy confirmed female mice exhibited superior organelle activity. Mitochondrial ATP synthesis rates of Holstein cows correlated (+.30 to +.48) with milk production traits of cows and their dams suggested maternal breeding values for milk yield might be improved by considering mitochondrial effects. No breed differences in state 3 respiration (17.7 ± 0.6 μM O2/mg protein/min) or ADP:O ratio with succinate (1.17 ± 0.01 μM ADP/μA O) existed among Angus, Brangus and Hereford cows. Regression analyses of growth traits of cows and their relatives on mitochondrial parameters revealed mainly nonsignificant mitochondrial effects. Significant regression coefficients (-0.43 to -1.05) were found for some cattle growth traits regressed on ADP:O ratios. No mitochondrial complementation occurred between neutrally-combining animal strains. Complementation occurred in mitochondrial mixtures from females of mouse strains with positive combining ability exclusively. Cow mitochondrial mixtures had lower (P < .05) state 3 rates than predicted. Advisors/Committee Members: DeNise, S. K (advisor), Allen, Ronald E. (committeemember), Ray, Donald E. (committeemember), Reid, B. L. (committeemember), McDaniel, Robert G. (committeemember).

Subjects/Keywords: Mitochondria.

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APA (6^th Edition):

Brown, D. R. (1987). GENETIC VARIATION IN MITOCHONDRIAL RESPIRATORY METABOLISM IN AVIAN AND MAMMALIAN SPECIES. (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/184046

Chicago Manual of Style (16^th Edition):

Brown, Daniel Robert. “GENETIC VARIATION IN MITOCHONDRIAL RESPIRATORY METABOLISM IN AVIAN AND MAMMALIAN SPECIES. ” 1987. Doctoral Dissertation, University of Arizona. Accessed February 25, 2020. http://hdl.handle.net/10150/184046.

MLA Handbook (7^th Edition):

Brown, Daniel Robert. “GENETIC VARIATION IN MITOCHONDRIAL RESPIRATORY METABOLISM IN AVIAN AND MAMMALIAN SPECIES. ” 1987. Web. 25 Feb 2020.

Vancouver:

Brown DR. GENETIC VARIATION IN MITOCHONDRIAL RESPIRATORY METABOLISM IN AVIAN AND MAMMALIAN SPECIES. [Internet] [Doctoral dissertation]. University of Arizona; 1987. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/10150/184046.

Council of Science Editors:

Brown DR. GENETIC VARIATION IN MITOCHONDRIAL RESPIRATORY METABOLISM IN AVIAN AND MAMMALIAN SPECIES. [Doctoral Dissertation]. University of Arizona; 1987. Available from: http://hdl.handle.net/10150/184046

University of Ottawa

14. Mazier, Hannah. Role of Mitochondrial Dynamics and Cell Death in a Dihydrotestosterone-induced Rat Model of Polycystic Ovarian Syndrome, and its Regulation by Gonadotropin .

Degree: 2016, University of Ottawa

URL: http://hdl.handle.net/10393/35572

► Polycystic ovarian syndrome (PCOS) is a multi-factorial infertility disorder whose etiology and pathogenesis is not completely understood. Although there is an association between dysregulation of… (more)

Subjects/Keywords: Reproduction; Mitochondria

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APA (6^th Edition):

Mazier, H. (2016). Role of Mitochondrial Dynamics and Cell Death in a Dihydrotestosterone-induced Rat Model of Polycystic Ovarian Syndrome, and its Regulation by Gonadotropin . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/35572

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Mazier, Hannah. “Role of Mitochondrial Dynamics and Cell Death in a Dihydrotestosterone-induced Rat Model of Polycystic Ovarian Syndrome, and its Regulation by Gonadotropin .” 2016. Thesis, University of Ottawa. Accessed February 25, 2020. http://hdl.handle.net/10393/35572.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Mazier, Hannah. “Role of Mitochondrial Dynamics and Cell Death in a Dihydrotestosterone-induced Rat Model of Polycystic Ovarian Syndrome, and its Regulation by Gonadotropin .” 2016. Web. 25 Feb 2020.

Vancouver:

Mazier H. Role of Mitochondrial Dynamics and Cell Death in a Dihydrotestosterone-induced Rat Model of Polycystic Ovarian Syndrome, and its Regulation by Gonadotropin . [Internet] [Thesis]. University of Ottawa; 2016. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/10393/35572.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mazier H. Role of Mitochondrial Dynamics and Cell Death in a Dihydrotestosterone-induced Rat Model of Polycystic Ovarian Syndrome, and its Regulation by Gonadotropin . [Thesis]. University of Ottawa; 2016. Available from: http://hdl.handle.net/10393/35572

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Adelaide

15. Day, David Alexander. Oxidative pathways of isolated plant mitochrondria.

Degree: 1975, University of Adelaide

URL: http://hdl.handle.net/2440/20040

Subjects/Keywords: Mitochondria.

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APA (6^th Edition):

Day, D. A. (1975). Oxidative pathways of isolated plant mitochrondria. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/20040

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Day, David Alexander. “Oxidative pathways of isolated plant mitochrondria.” 1975. Thesis, University of Adelaide. Accessed February 25, 2020. http://hdl.handle.net/2440/20040.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Day, David Alexander. “Oxidative pathways of isolated plant mitochrondria.” 1975. Web. 25 Feb 2020.

Vancouver:

Day DA. Oxidative pathways of isolated plant mitochrondria. [Internet] [Thesis]. University of Adelaide; 1975. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/2440/20040.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Day DA. Oxidative pathways of isolated plant mitochrondria. [Thesis]. University of Adelaide; 1975. Available from: http://hdl.handle.net/2440/20040

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Harvard University

16. Roach, Allie M. An Approach to Evaluate Inhibition of Cyclophilin D-Sensitive Mitochondrial Permeability Transition Pore Formation in Chronic Kidney Disease.

Degree: ALM, 2018, Harvard University

URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42003192

►

The mitochondrial permeability transition pore (mPTP) contributes to pathological outcomes in various contexts of tissue injury and disease involving mitochondrial perturbation, including in the kidneys.… (more)

Subjects/Keywords: Nephrology; Mitochondria

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APA (6^th Edition):

Roach, A. M. (2018). An Approach to Evaluate Inhibition of Cyclophilin D-Sensitive Mitochondrial Permeability Transition Pore Formation in Chronic Kidney Disease. (Masters Thesis). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:42003192

Chicago Manual of Style (16^th Edition):

Roach, Allie M. “An Approach to Evaluate Inhibition of Cyclophilin D-Sensitive Mitochondrial Permeability Transition Pore Formation in Chronic Kidney Disease.” 2018. Masters Thesis, Harvard University. Accessed February 25, 2020. http://nrs.harvard.edu/urn-3:HUL.InstRepos:42003192.

MLA Handbook (7^th Edition):

Roach, Allie M. “An Approach to Evaluate Inhibition of Cyclophilin D-Sensitive Mitochondrial Permeability Transition Pore Formation in Chronic Kidney Disease.” 2018. Web. 25 Feb 2020.

Vancouver:

Roach AM. An Approach to Evaluate Inhibition of Cyclophilin D-Sensitive Mitochondrial Permeability Transition Pore Formation in Chronic Kidney Disease. [Internet] [Masters thesis]. Harvard University; 2018. [cited 2020 Feb 25]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42003192.

Council of Science Editors:

Roach AM. An Approach to Evaluate Inhibition of Cyclophilin D-Sensitive Mitochondrial Permeability Transition Pore Formation in Chronic Kidney Disease. [Masters Thesis]. Harvard University; 2018. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42003192

17. Vusse, Ger. The role of mitochondria in testicular steroid production.

Degree: 1975, Erasmus University Medical Center

URL: http://hdl.handle.net/1765/31391

► textabstractThe testicular gland is the main androgen producing organ in male animals. The production of androgens is regulated by LH, secreted by the pituitary. The… (more)

Subjects/Keywords: mitochondria

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APA (6^th Edition):

Vusse, G. (1975). The role of mitochondria in testicular steroid production. (Doctoral Dissertation). Erasmus University Medical Center. Retrieved from http://hdl.handle.net/1765/31391

Chicago Manual of Style (16^th Edition):

Vusse, Ger. “The role of mitochondria in testicular steroid production.” 1975. Doctoral Dissertation, Erasmus University Medical Center. Accessed February 25, 2020. http://hdl.handle.net/1765/31391.

MLA Handbook (7^th Edition):

Vusse, Ger. “The role of mitochondria in testicular steroid production.” 1975. Web. 25 Feb 2020.

Vancouver:

Vusse G. The role of mitochondria in testicular steroid production. [Internet] [Doctoral dissertation]. Erasmus University Medical Center; 1975. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1765/31391.

Council of Science Editors:

Vusse G. The role of mitochondria in testicular steroid production. [Doctoral Dissertation]. Erasmus University Medical Center; 1975. Available from: http://hdl.handle.net/1765/31391

Columbia University

18. Garcia, Christian Joel. The Regulation of Mitochondrial Complex I Biogenesis in Drosophila Flight Muscles.

Degree: 2020, Columbia University

URL: https://doi.org/10.7916/d8-sg7a-7m23

► Mitochondrial Complex I (CI) is composed of 44 distinct subunits that are assembled with eight Fe- S clusters and a single flavin mononucleotide. Mitochondria is… (more)

Subjects/Keywords: Physiology; Biochemistry; Drosophila melanogaster; Mitochondria; Mitochondria – Formation

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APA (6^th Edition):

Garcia, C. J. (2020). The Regulation of Mitochondrial Complex I Biogenesis in Drosophila Flight Muscles. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/d8-sg7a-7m23

Chicago Manual of Style (16^th Edition):

Garcia, Christian Joel. “The Regulation of Mitochondrial Complex I Biogenesis in Drosophila Flight Muscles.” 2020. Doctoral Dissertation, Columbia University. Accessed February 25, 2020. https://doi.org/10.7916/d8-sg7a-7m23.

MLA Handbook (7^th Edition):

Garcia, Christian Joel. “The Regulation of Mitochondrial Complex I Biogenesis in Drosophila Flight Muscles.” 2020. Web. 25 Feb 2020.

Vancouver:

Garcia CJ. The Regulation of Mitochondrial Complex I Biogenesis in Drosophila Flight Muscles. [Internet] [Doctoral dissertation]. Columbia University; 2020. [cited 2020 Feb 25]. Available from: https://doi.org/10.7916/d8-sg7a-7m23.

Council of Science Editors:

Garcia CJ. The Regulation of Mitochondrial Complex I Biogenesis in Drosophila Flight Muscles. [Doctoral Dissertation]. Columbia University; 2020. Available from: https://doi.org/10.7916/d8-sg7a-7m23

Texas A&M University

19. Pratt, Anthony Thomas. Functional and Regulatory Studies of Cytochrome c Oxidase Assembly Factor 6.

Degree: 2015, Texas A&M University

URL: http://hdl.handle.net/1969.1/155711

► The mitochondrial respiratory chain (MRC) consists of four multi-protein complexes in the inner membrane of mitochondria and is the main site of cellular respiration. MRC… (more)

Subjects/Keywords: Coa6; yeast; mitochondria

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APA (6^th Edition):

Pratt, A. T. (2015). Functional and Regulatory Studies of Cytochrome c Oxidase Assembly Factor 6. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/155711

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Pratt, Anthony Thomas. “Functional and Regulatory Studies of Cytochrome c Oxidase Assembly Factor 6.” 2015. Thesis, Texas A&M University. Accessed February 25, 2020. http://hdl.handle.net/1969.1/155711.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Pratt, Anthony Thomas. “Functional and Regulatory Studies of Cytochrome c Oxidase Assembly Factor 6.” 2015. Web. 25 Feb 2020.

Vancouver:

Pratt AT. Functional and Regulatory Studies of Cytochrome c Oxidase Assembly Factor 6. [Internet] [Thesis]. Texas A&M University; 2015. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1969.1/155711.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Pratt AT. Functional and Regulatory Studies of Cytochrome c Oxidase Assembly Factor 6. [Thesis]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/155711

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Oregon State University

20. Wernick, Riana I. Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans.

Degree: PhD, Zoology, 2016, Oregon State University

URL: http://hdl.handle.net/1957/59186

► Understanding the impact of mitochondrial dysfunction on genome evolution has the potential not only to provide new insights on the basic evolutionary processes influencing mitochondrial… (more)

▼ Understanding the impact of mitochondrial dysfunction on genome evolution has the potential not only to provide new insights on the basic evolutionary processes influencing mitochondrial and nuclear genomes, but may also reveal novel avenues for evolutionary adaptive recovery from harmful mutations. Aberrant mitochondrial activity is fundamental to the pathology of mitochondrial diseases in addition to neurodegenerative disorders. While the effects of mitochondrial dysfunction have received much attention, less is known about their impact on genome evolution and potential target mechanisms for ameliorating the harmful effects of mitochondrial impairment. Characterizing genome modifications in animal populations predisposed to mitochondrial dysfunction may identify novel genes, mechanisms, and physiological pathways to target for recovery and provides a genome-wide perspective on the impact of aberrant mitochondrial activity. This dissertation research investigates how mitochondrial and nuclear genomes evolve in organisms genetically predisposed to mitochondrial dysfunction and contrasts genomic evolution in large and small population sizes. This work furthers understanding of the impact of evolutionary forces which influence genome evolution in population with reduced fitness, and reveals new insights into genomic responses to mitochondrial dysfunction. Chapters 2 and 3 of this dissertation focus on genome evolution using a set of mitochondrial respiratory chain mutant (gas-1¬ strain) and wild-type (N2 strain) Caenorhabditis elegans mutation-accumulation (MA) lines that experienced single-worm bottlenecking. The N2 MA lines, derived from a previous experiment, were bottlenecked for 250 generations. The gas-1 MA lines were created for this research, and bottlenecked in the laboratory for a maximum of 50 generations. Chapter 2 investigates mitogenomic evolution and heteroplasmic inheritance patterns evolving under extreme drift in gas-1 and N2 MA lines. Chapter 3 analyzes nuclear genome evolution using this same set of gas-1 and N2 MA lines. In contrast, Chapter 4 provides a complementary perspective, analyzing mitochondrial and nuclear genome evolution in twenty-four gas-1 'recovery line' (RC) populations, evolved in large population sizes for sixty generations. Bioinformatic methods and computational simulations were applied to characterize and evaluate genome evolution and provide a comprehensive investigation of the impact of mitochondrial dysfunction within a population genetics framework. In Chapter 2 our results of inherited mitochondrial DNA (mtDNA) heteroplasmy are in alignment with predictions of theories where a small subset of mtDNA molecules from the parental generation repopulates the mitochondrial genome pool for the progeny. Comparisons between Chapter 2 and 4 suggest that in both gas-1 and N2 strains organelle genome copy number is elevated in an environment characterized with extreme genetic drift but is less impacted throughout evolution in large populations when the force of genetic drift is… Advisors/Committee Members: Denver, Dee R. (advisor), Perez, Viviana (committee member).

Subjects/Keywords: Mitochondria; Caenorhabditis elegans

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APA (6^th Edition):

Wernick, R. I. (2016). Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/59186

Chicago Manual of Style (16^th Edition):

Wernick, Riana I. “Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans.” 2016. Doctoral Dissertation, Oregon State University. Accessed February 25, 2020. http://hdl.handle.net/1957/59186.

MLA Handbook (7^th Edition):

Wernick, Riana I. “Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans.” 2016. Web. 25 Feb 2020.

Vancouver:

Wernick RI. Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans. [Internet] [Doctoral dissertation]. Oregon State University; 2016. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1957/59186.

Council of Science Editors:

Wernick RI. Evolutionary Genomic Responses to Mitochondrial Dysfunction in Caenorhabditis elegans. [Doctoral Dissertation]. Oregon State University; 2016. Available from: http://hdl.handle.net/1957/59186

University of Hong Kong

21. Verma, Deepika. Study of cysteine and cystine transport in plant mitochondria.

Degree: PhD, 2015, University of Hong Kong

URL: Verma, D.. (2015). Study of cysteine and cystine transport in plant mitochondria. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5760949 ; http://hdl.handle.net/10722/226746

► Cysteine biosynthesis plays an important role in plants for sulfur assimilation. Cysteine regulates the detoxification of cyanide that is a respiratory inhibitor generated mainly during… (more)

▼ Cysteine biosynthesis plays an important role in plants for sulfur assimilation. Cysteine regulates the detoxification of cyanide that is a respiratory inhibitor generated mainly during ethylene biosynthesis in higher plants. Cyanide detoxification occurs by the ß-substitution of the sulfhydryl of cysteine with cyanide catalyzed into β-cyanoalanine by the ß-cyanoalanine synthase (β-CAS) enzyme in the mitochondria. In plants and bacteria two enzymes catalyze the synthesis of cysteine; serine acetyltransferase (SAT) transfer acetyl- CoA to serine, generating oacetylserine (OAS) which further combines with sulfide ion to form cysteine, the latter reaction is catalyzed by O-acetyl serine sulfhydrylase (OASS). SAT and OASS associate to form cysteine synthase complex (CSC). The isoforms of SAT and OASS have been found in the cytosol, plastids, and mitochondria of several dicotyledonous plants. The function of cysteine synthesis at various sites and its transport within the compartments of the cell is ambiguous. Two type of dicot plant material, wild-type (WT) Arabidopsis thaliana and pear fruits that are distinct in nature, family and origin were selected for this research. Pears are pomaceous fruits that produce a large amount of ethylene during fruit ripening. The selection of fruit material was based on its ethylene measurements. WT Arabidopsis was grown on MS medium and 15-20 days old rosettes were used for the experimental purpose. The mitochondria from both types of plants were isolated and purified using continuous percoll gradient. It was used for respirometry, liquid scintillation counting, and liquid chromatography-tandem mass spectroscopy (LC-MS/MS) assays. The analysis of quality of mitochondria was based on respiratory control ratio, coupling, ADP: O ratio and cytochrome C oxidase latency test. According to oxygraph assays, cyanide inhibits the respiration process, but the application of L-cysteine as low as 5μM in pear and 10μM L-cysteine in Arabidopsis mitochondria can protect the rate of respiration and assist in cyanide detoxification. 2.5μM cystine also shows the similar effect as tested for pear mitochondria. Cyanide concentration required for total inhibition of respiration range between 10 μM to 100 μM. Amino-oxyacetic acid assay suggested that β-cyanoalanine synthase signals the mitochondrial transport of cysteine and cystine. Dithiothreitol (DTT) reduction and Nethylmaleimide (NEM) assay inferred that cysteine is a preferred substrate for cyanide detoxification. Respirometry analysis shows that L-glutamic acid competes with both cysteine and cystine, and aspartic acid interferes with transportation of cystine more than that of cysteine. The specific inhibitors of Xag transport system (AβH, i.e., aspartic-β-hydroxamate) and Xc system (quisqualic acid, S-4-Carboxyphenylglycine (CPG)) inhibit the cysteine and cystine transport in pears. These inhibitors were further tested in liquid scintillation counting by using Lcysteine S³⁵ radioisotope and LC-MS/MS experiments by estimating β-cyanoalanine…

Subjects/Keywords: Cysteine; Plant mitochondria

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APA (6^th Edition):

Verma, D. (2015). Study of cysteine and cystine transport in plant mitochondria. (Doctoral Dissertation). University of Hong Kong. Retrieved from Verma, D.. (2015). Study of cysteine and cystine transport in plant mitochondria. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5760949 ; http://hdl.handle.net/10722/226746

Chicago Manual of Style (16^th Edition):

Verma, Deepika. “Study of cysteine and cystine transport in plant mitochondria.” 2015. Doctoral Dissertation, University of Hong Kong. Accessed February 25, 2020. Verma, D.. (2015). Study of cysteine and cystine transport in plant mitochondria. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5760949 ; http://hdl.handle.net/10722/226746.

MLA Handbook (7^th Edition):

Verma, Deepika. “Study of cysteine and cystine transport in plant mitochondria.” 2015. Web. 25 Feb 2020.

Vancouver:

Verma D. Study of cysteine and cystine transport in plant mitochondria. [Internet] [Doctoral dissertation]. University of Hong Kong; 2015. [cited 2020 Feb 25]. Available from: Verma, D.. (2015). Study of cysteine and cystine transport in plant mitochondria. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5760949 ; http://hdl.handle.net/10722/226746.

Council of Science Editors:

Verma D. Study of cysteine and cystine transport in plant mitochondria. [Doctoral Dissertation]. University of Hong Kong; 2015. Available from: Verma, D.. (2015). Study of cysteine and cystine transport in plant mitochondria. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5760949 ; http://hdl.handle.net/10722/226746

University of Hawaii – Manoa

22. Brucks, Eric Snodgrass. Metagenome recruitment of the global ocean survey dataset to four closely-related SAR11 genomes.

Degree: 2015, University of Hawaii – Manoa

URL: http://hdl.handle.net/10125/100300

►

M.S. University of Hawaii at Manoa 2014.

The free-living marine bacterial clade known as SAR11 is thought to be one of the most abundant lineages… (more)

Subjects/Keywords: marine; mitochondria; bacteria

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APA (6^th Edition):

Brucks, E. S. (2015). Metagenome recruitment of the global ocean survey dataset to four closely-related SAR11 genomes. (Thesis). University of Hawaii – Manoa. Retrieved from http://hdl.handle.net/10125/100300

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Brucks, Eric Snodgrass. “Metagenome recruitment of the global ocean survey dataset to four closely-related SAR11 genomes.” 2015. Thesis, University of Hawaii – Manoa. Accessed February 25, 2020. http://hdl.handle.net/10125/100300.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Brucks, Eric Snodgrass. “Metagenome recruitment of the global ocean survey dataset to four closely-related SAR11 genomes.” 2015. Web. 25 Feb 2020.

Vancouver:

Brucks ES. Metagenome recruitment of the global ocean survey dataset to four closely-related SAR11 genomes. [Internet] [Thesis]. University of Hawaii – Manoa; 2015. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/10125/100300.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Brucks ES. Metagenome recruitment of the global ocean survey dataset to four closely-related SAR11 genomes. [Thesis]. University of Hawaii – Manoa; 2015. Available from: http://hdl.handle.net/10125/100300

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Minnesota

23. Visweswaran, Ramjay. The importance of calcium cycling and mitochondria in the local onset of alternans in the heart.

Degree: PhD, Biomedical Engineering, 2014, University of Minnesota

URL: http://hdl.handle.net/11299/165107

► Action potential duration (APD) alternans can be accompanied by alternans in intracellular calcium, leading to electromechanical alternans. Electromechanical alternans is considered a substrate for ventricular… (more)

▼ Action potential duration (APD) alternans can be accompanied by alternans in intracellular calcium, leading to electromechanical alternans. Electromechanical alternans is considered a substrate for ventricular fibrillation, especially during pathophysiological conditions such as ischemia. The work in thesis seeks to elucidate the spatio-temporal evolution of alternans and to investigate the potential pathways through which they occur. High resolution mapping was used to simultaneously map membrane voltage and intracellular calcium in normal rabbit hearts. By mapping both parameters simultaneously in the same region of the heart, we were able to reveal that instability in calcium cycling plays a primary role in the development of EM alternans in the whole heart. Further, we were able to apply a special restitution portrait analysis to predict the onset of both calcium and APD alternans before it occurs. We also wanted to elucidate the mechanisms behind the increased incidences of arrhythmias during ischemia. By simulating ischemic and mitochondrial dysfunction in isolated rabbit hearts, we were able to show that mitochondrial stress caused by uncoupling of the mitochondria is responsible for early occurrence of both APD and calcium alternans in the heart, which in turn creates a substrate to ventricular arrhythmias. Thus, uncoupling of the mitochondrial network that occurs during ischemia might be the primary reason for increased incidences of arrhythmias in the heart during ischemia. Overall, this study improves our knowledge of alternans and their basic underlying mechanism which can be used in the development of better treatment and/or prevention strategies. Development of techniques to predict alternans before it occurs would be a valuable clinical tool, especially for use in implantable pacemakers paving the way for pre-emptive interventions. In addition, elucidating the mechanism or pathways of alternans formation would lead to targeted drug treatments to prevent alternans and thus, VF and sudden cardiac death.

Subjects/Keywords: Alternans; Calcium; Mitochondria

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APA (6^th Edition):

Visweswaran, R. (2014). The importance of calcium cycling and mitochondria in the local onset of alternans in the heart. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/165107

Chicago Manual of Style (16^th Edition):

Visweswaran, Ramjay. “The importance of calcium cycling and mitochondria in the local onset of alternans in the heart.” 2014. Doctoral Dissertation, University of Minnesota. Accessed February 25, 2020. http://hdl.handle.net/11299/165107.

MLA Handbook (7^th Edition):

Visweswaran, Ramjay. “The importance of calcium cycling and mitochondria in the local onset of alternans in the heart.” 2014. Web. 25 Feb 2020.

Vancouver:

Visweswaran R. The importance of calcium cycling and mitochondria in the local onset of alternans in the heart. [Internet] [Doctoral dissertation]. University of Minnesota; 2014. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/11299/165107.

Council of Science Editors:

Visweswaran R. The importance of calcium cycling and mitochondria in the local onset of alternans in the heart. [Doctoral Dissertation]. University of Minnesota; 2014. Available from: http://hdl.handle.net/11299/165107

24. Poston, Chloe N. Mass Spectrometry-Based Global Proteomic Analysis of Endoplasmic Reticulum and Mitochondria Contact Sites.

Degree: PhD, Chemistry, 2013, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:320610/

► Mass spectrometry has been a long-standing analytical tool for chemists. Tandem mass spectrometry-based proteomics capitalizes on the sensitivity, accuracy, and efficiency of this classic technique… (more)

Subjects/Keywords: Mitochondria-Associated Membranes

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APA (6^th Edition):

Poston, C. N. (2013). Mass Spectrometry-Based Global Proteomic Analysis of Endoplasmic Reticulum and Mitochondria Contact Sites. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:320610/

Chicago Manual of Style (16^th Edition):

Poston, Chloe N. “Mass Spectrometry-Based Global Proteomic Analysis of Endoplasmic Reticulum and Mitochondria Contact Sites.” 2013. Doctoral Dissertation, Brown University. Accessed February 25, 2020. https://repository.library.brown.edu/studio/item/bdr:320610/.

MLA Handbook (7^th Edition):

Poston, Chloe N. “Mass Spectrometry-Based Global Proteomic Analysis of Endoplasmic Reticulum and Mitochondria Contact Sites.” 2013. Web. 25 Feb 2020.

Vancouver:

Poston CN. Mass Spectrometry-Based Global Proteomic Analysis of Endoplasmic Reticulum and Mitochondria Contact Sites. [Internet] [Doctoral dissertation]. Brown University; 2013. [cited 2020 Feb 25]. Available from: https://repository.library.brown.edu/studio/item/bdr:320610/.

Council of Science Editors:

Poston CN. Mass Spectrometry-Based Global Proteomic Analysis of Endoplasmic Reticulum and Mitochondria Contact Sites. [Doctoral Dissertation]. Brown University; 2013. Available from: https://repository.library.brown.edu/studio/item/bdr:320610/

University of Western Australia

25. Zhang, Botao. Functional characterization of mitochondrial stress response in Arabidopsis thaliana.

Degree: PhD, 2012, University of Western Australia

URL: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=33628&local_base=GEN01-INS01

►

[Truncated abstract] Plants, because of their immobile nature, are continually exposed to a variety of extreme environmental conditions i.e. stresses. Stresses have adverse effects on… (more)

▼

[Truncated abstract] Plants, because of their immobile nature, are continually exposed to a variety of extreme environmental conditions i.e. stresses. Stresses have adverse effects on plant growth, development and seed production. Nearly all biotic and abiotic stresses disrupt the metabolic balance of cells, resulting in osmotic stress and enhanced production of reactive oxygen species (ROS) (Mittler et al., 2004). Mitochondria are one of the major sources of ROS and a major target of oxidative stress, and are vital for maintaining the viability during biotic and abiotic stress. Previous studies showed that there are a number of mitochondrial proteins that are induced by different treatments directly targeted to mitochondria (Clifton et al., 2006). However, the response of mitochondria to stress and the roles mitochondria play under stress are still not very clear. In this study, the functional characterization of mitochondrial stress response was conducted. By combining a list of 1196 Arabidopsis thaliana genes that putatively encode mitochondrial proteins with 16 publicly available microarray datasets under stress conditions, 45 nuclear encoded proteins were defined as mitochondrial stress-responsive proteins. Furthermore, the mitochondrial localization of these proteins was tested using green fluorescent protein (GFP) fusion assays. In total 26 proteins could be confirmed to be targeted to mitochondria and were thus considered to be mitochondrial stress responsive proteins. Two of the mitochondrial stress responsive genes were selected for functional characterization. One of these proteins, AtLETM1 (leucine zipper-EF-hand-containing transmembrane protein), was investigated using T-DNA insertion lines. Analysis revealed the presence of a paralog in Arabidopsis. Inactivation of either AtLETM1 or AtLETM2 did not result in any severe deleterious growth phenotypes, while inactivation of both genes was lethal.

However, plants that are hemizygous for AtLETM2 and homozygous for AtLETM1 (letm1 (-/-) LETM2 (+/-)) showed a retarded growth phenotype during early seedling growth. Studies revealed that a functional maternal AtLETM2 allele in the absence of AtLETM1 was required for viability and was shown that the expression of paternal AtLETM2 allele was silenced during early embryogenesis. The translation rates in mitochondria of letm1 (-/-) LETM2 (+/-) plants were decreased, resulting in plants with reduced amounts of the α-subunit of mitochondrial ATP synthase and cytochrome c. The letm1 (-/-) LETM2(+/-) plants also displayed lower levels of ATP, increased total ascorbate levels and increased resistance to drought stress. These results show that AtLETM activity is essential for mitochondrial translation and its expression is under maternal control during early seed development. The second protein that was investigated was AtBCS1, an AAA-type ATPase. Subcellular localization assays confirmed its location in mitochondrial outer membrane. Phylogenetic and structural analysis indicated functional divergence between the plant…

Subjects/Keywords: Mitochondria; Stress; Function

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APA (6^th Edition):

Zhang, B. (2012). Functional characterization of mitochondrial stress response in Arabidopsis thaliana. (Doctoral Dissertation). University of Western Australia. Retrieved from http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=33628&local_base=GEN01-INS01

Chicago Manual of Style (16^th Edition):

Zhang, Botao. “Functional characterization of mitochondrial stress response in Arabidopsis thaliana.” 2012. Doctoral Dissertation, University of Western Australia. Accessed February 25, 2020. http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=33628&local_base=GEN01-INS01.

MLA Handbook (7^th Edition):

Zhang, Botao. “Functional characterization of mitochondrial stress response in Arabidopsis thaliana.” 2012. Web. 25 Feb 2020.

Vancouver:

Zhang B. Functional characterization of mitochondrial stress response in Arabidopsis thaliana. [Internet] [Doctoral dissertation]. University of Western Australia; 2012. [cited 2020 Feb 25]. Available from: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=33628&local_base=GEN01-INS01.

Council of Science Editors:

Zhang B. Functional characterization of mitochondrial stress response in Arabidopsis thaliana. [Doctoral Dissertation]. University of Western Australia; 2012. Available from: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=33628&local_base=GEN01-INS01

Penn State University

26. Han, Min-Joon. MAMMALIAN MITOCHONDRIAL RIBOSOMAL PROTEINS :.

Degree: PhD, Biochemistry, Microbiology, and Molecular Biology, 2010, Penn State University

URL: https://etda.libraries.psu.edu/catalog/11017

► Human mitochondria are essential for cell survival while playing key roles in programmed cell death also called apoptosis. First of all, mitochondria are the main… (more)

▼ Human mitochondria are essential for cell survival while playing key roles in programmed cell death also called apoptosis. First of all, mitochondria are the main source of energy for the eukaryotic cell. Mitochondria produce more than 90% of the energy used by mammalian cells in a process referred to as oxidative phosphorylation. This demanding mechanism requires a lot of proteins, which are nucleus-encoded, synthesized in cytoplasm, and imported into mitochondria. However, it also requires 13 mitochondrial-encoded proteins. Mitochondria have their own 16.5 kb circular genome (mtDNA) and ribosome to translate these 13 proteins. Even though mammalian mitochondrial ribosomes (55S) differ from bacterial (70S) and mammalian cytoplasmic ribosomes (80S), many of the mitochondrial ribosomal proteins have bacterial homologs and similar functions. Some of the mitochondrial ribosomal proteins, which have no homologs in bacterial ribosomes, are involved in the process of apoptosis. Therefore, mitochondrial ribosome is essential not only for the translation of 13 proteins for energy production but also the regulation of apoptosis. Here, two regulatory mechanisms involved in mitochondrial functions by mitochondrial ribosomal proteins were investigated; energy production by OXPHOS and apoptosis. First, we reported that the presence of different splice variants of MRPS29, which contained an uORF in the 5'-UTR in humans and the expression of MRPS29 could be translationally controlled by the uORF found in the 5'-UTR. Data presented in this thesis also suggest that reduction in MRPS29 expression by uORF may inhibit MRPS29-induced apoptosis. Therefore, the presence of uORF-MRPS29 mRNAs in human potentially indicates a new mechanism for regulation of apoptosis. Another regulatory mechanism via post-translational modification has been revealed by studying mitochondrial ribosomal L7/L12 stalk region. The mitochondrial ribosomal protein L10 (MRPL10) was identified as a major acetylated protein in the mitochondrial ribosome. We also found that ribosome associated SIRT3 was responsible for deacetylation of MRPL10 in a NAD+-dependent manner. A mechanism by which the mitochondrial translation is regulated by reversible acetylation is proposed. Increased acetylation status of mitochondrial ribosome in SIRT3 knock-out (Sirt3-/-) mice enhanced MRPL12 binding to the ribosome and recruitment of elongation factors to increase translation. On the other hand, over-expression of SIRT3 reduced the translation and MRPL12 binding to ribosomes by deacetylation of the mitochondrial ribosome. Therefore, acetylation of MRPL10 due to inhibition of SIRT3 could enhance its interaction with MRPL12, resulting in increased MRPL12 binding to ribosomes and the recruitment of elongation factors during translation. These findings constitute the first evidence for the regulation of mitochondrial protein synthesis through the reversible acetylation of the mitochondrial ribosome and identified MRPL10 as a novel substrate of NAD+-dependent deacetylase, SIRT3.

Subjects/Keywords: translation; mitochondria; apoptosis

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APA (6^th Edition):

Han, M. (2010). MAMMALIAN MITOCHONDRIAL RIBOSOMAL PROTEINS :. (Doctoral Dissertation). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/11017

Chicago Manual of Style (16^th Edition):

Han, Min-Joon. “MAMMALIAN MITOCHONDRIAL RIBOSOMAL PROTEINS :.” 2010. Doctoral Dissertation, Penn State University. Accessed February 25, 2020. https://etda.libraries.psu.edu/catalog/11017.

MLA Handbook (7^th Edition):

Han, Min-Joon. “MAMMALIAN MITOCHONDRIAL RIBOSOMAL PROTEINS :.” 2010. Web. 25 Feb 2020.

Vancouver:

Han M. MAMMALIAN MITOCHONDRIAL RIBOSOMAL PROTEINS :. [Internet] [Doctoral dissertation]. Penn State University; 2010. [cited 2020 Feb 25]. Available from: https://etda.libraries.psu.edu/catalog/11017.

Council of Science Editors:

Han M. MAMMALIAN MITOCHONDRIAL RIBOSOMAL PROTEINS :. [Doctoral Dissertation]. Penn State University; 2010. Available from: https://etda.libraries.psu.edu/catalog/11017

University of Aberdeen

27. Al-Tarrah, Mustafa. The effect of citrate synthase on skeletal muscle metabolism.

Degree: PhD, 2017, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=235778 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.737930

► Citrate synthase (CS) is a key mitochondrial enzyme in the tricarboxylic acid cycle (TCA). TCA provides NADH and FADH for the ETC to generate ATP… (more)

▼ Citrate synthase (CS) is a key mitochondrial enzyme in the tricarboxylic acid cycle (TCA). TCA provides NADH and FADH for the ETC to generate ATP through oxidative phosphorylation in muscle cells. The aim of this PhD project is to investigate the role of CS in skeletal muscle metabolism. The aim of the first study was to investigate the effects of a high fat diet (HFD, 45 % kcal fat) for 12 weeks on CS activity in the heart and gastrocnemius muscle of C57BL/6J (B6) mice and congenic (B6.A) characterised by 39% reduced CS activity. Spectrophotometric analysis of CS activity in the heart and gastrocnemius muscle revealed that HFD led to an increase in CS activity in gastrocnemius muscle but a decrease in the heart in both strains of mice. The aim of the second study was to investigate the effects of low CS activity on substrate metabolism in primary muscle cells established from B6 and B6.A mice. Primary muscle cells from both strains were incubated in radiolabelled glucose or palmitate to assess their oxidation in the mitochondria. The reduction of CS activity in B6.A muscle cells did not affect glucose and palmitate oxidation. The aim of the third study was to investigate the effects of D- and L-serine on CS activity in B6 muscle homogenates, primary muscle cells and purified CS from porcine heart. The muscle samples were incubated in D - or L-serine at 0.1 mM or 5 mM concentration and CS activity levels were assessed by spectrophotometer. D- or L-serine did not have any effect on CS activity in muscle samples. The aim of the fourth study was to investigate the effects of low CS activity on substrate metabolism in C2C12 muscle cells. Lentiviral transduction of C2C12 muscle cells with shRNA resulted in a reduction of CS activity and the metabolic pathways were assessed using XF24 Analyser, western blotting, Immunofluorescence and qRTPCR. Low CS activity was associated with a reduction in substrate oxidation by the mitochondria, an increase in glycolysis and ceramide accumulation in C2C12 muscle cells. The results highlight the significance of CS activity as a modulator of muscle metabolism.

Subjects/Keywords: Mitochondria; Enzymes; Muscles

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APA (6^th Edition):

Al-Tarrah, M. (2017). The effect of citrate synthase on skeletal muscle metabolism. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=235778 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.737930

Chicago Manual of Style (16^th Edition):

Al-Tarrah, Mustafa. “The effect of citrate synthase on skeletal muscle metabolism.” 2017. Doctoral Dissertation, University of Aberdeen. Accessed February 25, 2020. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=235778 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.737930.

MLA Handbook (7^th Edition):

Al-Tarrah, Mustafa. “The effect of citrate synthase on skeletal muscle metabolism.” 2017. Web. 25 Feb 2020.

Vancouver:

Al-Tarrah M. The effect of citrate synthase on skeletal muscle metabolism. [Internet] [Doctoral dissertation]. University of Aberdeen; 2017. [cited 2020 Feb 25]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=235778 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.737930.

Council of Science Editors:

Al-Tarrah M. The effect of citrate synthase on skeletal muscle metabolism. [Doctoral Dissertation]. University of Aberdeen; 2017. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=235778 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.737930

Latrobe University

28. Palmer, Catherine Sarah. MiD49 and MiD51 : new mediators of mitochondrial division.

Degree: PhD, 2012, Latrobe University

URL: http://hdl.handle.net/1959.9/530588

►

Thesis (Ph.D.) - La Trobe University, 2012

Submission note: "A thesis submitted in total fulfilment of the requirement for the degree of Doctor of Philosophy… (more)

Subjects/Keywords: Mitochondria.; Microbiology.; Proteins.

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APA (6^th Edition):

Palmer, C. S. (2012). MiD49 and MiD51 : new mediators of mitochondrial division. (Doctoral Dissertation). Latrobe University. Retrieved from http://hdl.handle.net/1959.9/530588

Chicago Manual of Style (16^th Edition):

Palmer, Catherine Sarah. “MiD49 and MiD51 : new mediators of mitochondrial division.” 2012. Doctoral Dissertation, Latrobe University. Accessed February 25, 2020. http://hdl.handle.net/1959.9/530588.

MLA Handbook (7^th Edition):

Palmer, Catherine Sarah. “MiD49 and MiD51 : new mediators of mitochondrial division.” 2012. Web. 25 Feb 2020.

Vancouver:

Palmer CS. MiD49 and MiD51 : new mediators of mitochondrial division. [Internet] [Doctoral dissertation]. Latrobe University; 2012. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/1959.9/530588.

Council of Science Editors:

Palmer CS. MiD49 and MiD51 : new mediators of mitochondrial division. [Doctoral Dissertation]. Latrobe University; 2012. Available from: http://hdl.handle.net/1959.9/530588

Boston University

29. McLoed, Melissa. THE mitochondrial uniporter modulates neuronal regenerative outgrowth and calcium dynamics following axotomy in C. elegans.

Degree: 2015, Boston University

URL: http://hdl.handle.net/2144/13983

► Following neuronal injury, calcium signaling plays a critical role in promoting repair processes. Injury produces an initial cytosolic calcium elevation mediated by calcium entry from… (more)

Subjects/Keywords: Neurosciences; Calcium; Mitochondria

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APA (6^th Edition):

McLoed, M. (2015). THE mitochondrial uniporter modulates neuronal regenerative outgrowth and calcium dynamics following axotomy in C. elegans. (Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/13983

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

McLoed, Melissa. “THE mitochondrial uniporter modulates neuronal regenerative outgrowth and calcium dynamics following axotomy in C. elegans.” 2015. Thesis, Boston University. Accessed February 25, 2020. http://hdl.handle.net/2144/13983.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

McLoed, Melissa. “THE mitochondrial uniporter modulates neuronal regenerative outgrowth and calcium dynamics following axotomy in C. elegans.” 2015. Web. 25 Feb 2020.

Vancouver:

McLoed M. THE mitochondrial uniporter modulates neuronal regenerative outgrowth and calcium dynamics following axotomy in C. elegans. [Internet] [Thesis]. Boston University; 2015. [cited 2020 Feb 25]. Available from: http://hdl.handle.net/2144/13983.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

McLoed M. THE mitochondrial uniporter modulates neuronal regenerative outgrowth and calcium dynamics following axotomy in C. elegans. [Thesis]. Boston University; 2015. Available from: http://hdl.handle.net/2144/13983

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Cambridge

30. Gaude, Edoardo. Mitochondrial metabolism in cancer transformation and progression.

Degree: PhD, 2018, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/275090

► Cancer cells undergo a multifaceted rewiring of cellular metabolism to support their biosynthetic needs. Although the major determinants of this metabolic transformation have been elucidated,… (more)

▼ Cancer cells undergo a multifaceted rewiring of cellular metabolism to support their biosynthetic needs. Although the major determinants of this metabolic transformation have been elucidated, their broad biological implications and clinical relevance are unclear. In this study, I systematically analysed the expression of metabolic genes across 20 different cancer types and investigated their impact on clinical outcome. I found that cancers undergo a tissue-specific metabolic rewiring, which converges towards a common metabolic landscape. Of note, downregulation of mitochondrial genes is associated with the worst clinical outcome across all cancer types and correlates with the expression of epithelial-to-mesenchymal transition (EMT) gene signature, a feature of invasive and metastatic cancers. Consistently, suppression of mitochondrial genes is identified as key metabolic signature of metastatic melanoma and renal cancer, and metastatic cell lines. This comprehensive analysis reveals unexpected facets of cancer metabolism, with important implications for cancer patients stratification, prognosis, and therapy. I then investigated how mitochondrial dysfunction could affect cell behaviour. I capitalised on a recently developed in vitro cell model with increasing levels of m.8993T>G mutation heteroplasmy. I found that impaired utilisation of reduced nicotinamide adenine dinucleotide (NADH) by the mitochondrial respiratory chain leads to cytosolic reductive carboxylation of glutamine as a new mechanism for cytosol-confined NADH recycling supported by malate dehydrogenase 1 (MDH1). This metabolic coupling is facilitated by the formation of a multienzymatic complex between MDH1 and GAPDH. Importantly, such metabolic coupling between glutamine metabolism and cytosolic NADH recycling is able to support increased glycolytic flux, an important hallmark of cells with dysfunctional mitochondria, as well as cancer cells. Finally, increased glycolysis in cells with mitochondrial dysfunction is associated with enhanced cell migration, in an MDH1-dependent fashion. These results describe a novel link between glycolysis and mitochondrial dysfunction, and uncover potential targets for cells that rely on aerobic glycolysis for proliferation and migration, such as cancer cells.

Subjects/Keywords: Cancer; metabolism; mitochondria

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APA (6^th Edition):

Gaude, E. (2018). Mitochondrial metabolism in cancer transformation and progression. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/275090

Chicago Manual of Style (16^th Edition):

Gaude, Edoardo. “Mitochondrial metabolism in cancer transformation and progression.” 2018. Doctoral Dissertation, University of Cambridge. Accessed February 25, 2020. https://www.repository.cam.ac.uk/handle/1810/275090.

MLA Handbook (7^th Edition):

Gaude, Edoardo. “Mitochondrial metabolism in cancer transformation and progression.” 2018. Web. 25 Feb 2020.

Vancouver:

Gaude E. Mitochondrial metabolism in cancer transformation and progression. [Internet] [Doctoral dissertation]. University of Cambridge; 2018. [cited 2020 Feb 25]. Available from: https://www.repository.cam.ac.uk/handle/1810/275090.

Council of Science Editors:

Gaude E. Mitochondrial metabolism in cancer transformation and progression. [Doctoral Dissertation]. University of Cambridge; 2018. Available from: https://www.repository.cam.ac.uk/handle/1810/275090

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Open Access Theses and Dissertations