Tesi sul tema "Mitochondrial DNA"
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Al, Amir Dache Zahra. "Étude de la structure de l'ADN circulant d'origine mitochondriale". Thesis, Montpellier, 2019. http://www.theses.fr/2019MONTT059.
Testo completoPlasma transports blood cells with a mixture of compounds, including nutrients, waste, antibodies, and chemical messengers...throughout the body. Non-soluble factors such as circulating DNA and extracellular vesicles have recently been added to the list of these components and have been the subject of extensive research due to their role in intercellular communication. Circulating DNA (cirDNA) is composed of cell-free and particle-associated DNA fragments, which can be released by all cell types. cirDNA is derived not only from genomic DNA but also from extrachromosomal mitochondrial DNA. Numerous studies carried out lately indicate that the quantitative and qualitative analysis of cirDNA represents a breakthrough in clinical applications as a non-invasive biomarker for diagnosis, prognosis and therapeutic follow-up. However, despite the promising future of cirDNA in clinical applications, particularly in oncology, knowledge regarding its origins, composition and functions, that could considerably optimize its diagnostic value, is still lacking.The main goal of my thesis was to identify and characterize the structural properties of extracellular DNA of mitochondrial origin. By examining the integrity of this DNA, as well as the size and density of associated structures, this work revealed the presence of dense particles larger than 0.2 µm containing whole mitochondrial genomes. We characterized these structures by electron microscopy and flow cytometry and identified intact mitochondria in the extracellular medium in vitro and ex vivo (in plasma samples from healthy individuals). Oxygen consumption by these mitochondria was detected by the Seahorse technology, suggesting that at least some of these intact extracellular mitochondria may be functional.In addition, I contributed to other studies carried out in the team, such as studies aiming at evaluating (1) the influence of pre-analytical and demographic parameters on the quantification of nuclear and mitochondrial cirDNA on a cohort of 104 healthy individuals and 118 patients with metastatic colorectal cancer, (2) the influence of hypoxia on the release of cirDNA in vitro and in vivo, and (3) the potential of cirDNA analysis in the early detection and screening of cancer.This manuscript present a recent review on cirDNA and its different mechanisms of release, which go hand in hand with the structural characterization of this DNA, its functional aspects and its clinical applications. In addition, this thesis provides new knowledge on the structure of extracellular mitochondrial DNA and opens up new avenues for reflection, particularly on the potential impact that could have those circulating mitochondria on cell-cell communication, inflammation and clinical applications
Berg, Alonso Laetitia. "Déficits de la chaîne respiratoire mitochondriale avec instabilité de l’ADN mitochondrial : identification de nouveaux gènes et mécanismes". Thesis, Université Côte d'Azur (ComUE), 2016. http://www.theses.fr/2016AZUR4101/document.
Testo completoNon communiqué
Rebelo, Adriana. "Probing Mitochondrial DNA Structure with Mitochondria-Targeted DNA Methyltransferases". Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/344.
Testo completoBoyer, Hélène. "The mamalian circadian clock regulates the abundance and expression of mitochondrial DNA in the nuclear compartment". Thesis, Lyon, 2020. http://www.theses.fr/2020LYSEN015.
Testo completoThe mitochondrial genome is minimal and most of the mitochondrial proteins are encoded in the nuclear genome. Thus, although mitochondrial and nuclear genomes are physically separated in the cell, anterograde (nuclear to mitochondrial) and retrograde (mitochondrial to nuclear) signals are essential for mitochondrial biogenesis to be coordinated with the cellular energetic demands. Those demands are cyclical in nature, and the circadian clock regulates numerous aspects of mitochondrial biology, including the dynamics of fusion and fission that shape the architecture of the mitochondrial network. In murine livers, the network oscillates between fused (during the day) and fragmented structures (during the night). A fused network is associated with a more efficient ATP production whereas fragmentation is associated with elevated mitochondrial ROS levels and mitophagy. In other words, if mtDNA was to ever escape mitochondria, fission would help. Complementation experiments in yeast have shown that mitochondrial DNA (mtDNA) is able to escape from the mitochondria and enter the nucleus. In human cells (HeLa), the intact and full-length mitochondrial genome has been detected in the nucleus. Evolutionary analyses of nuclear inserted mitochondrial sequences (numts) suggest an ongoing process of integration of mitochondrial sequences into the nuclear genome. Also, abundant somatically acquired mitochondrial- nuclear genome fusion events (simts) have been shown to occur in human cancer cells - an extreme context of genomic instability and disrupted circadian rhythms. The availability of mtDNA in the cytoplasm, protected by vesicles, to be taken up by the nucleus is thought to result from mitophagy. As mitophagy and mitochondrial dynamics are regulated by the circadian clock, we investigated whether mtDNA would accumulate in the nuclear compartment as a function of circadian time. We addressed this question in the mouse liver, a differentiate mammalian tissue. This work demonstrates that the nuclear abundance of mtDNA in murine livers is regulated by the circadian clock – with a zenith at the end of the circadian night. Nuclear mtDNA is differentially hydroxymethylated relative to the total mtDNA extracted from the same tissue. Also, circadian clock disruption altered the phase and abundance of nuclear mtDNA. Additionally, we observed that concurrent accumulation of nuclear mtRNA was sensitive to nutritional challenges. Probably, these dynamics are driven by mitochondrial network remodeling dynamics. Increased nuclear presence and insertions of mtDNA in cancer cells or aging tissues, which are often associated with disrupted circadian oscillators- may thus arise from the loss of a physiological rhythm in mitochondrial-network remodeling
Korhonen, Jenny. "Functional and structural characterization of the human mitochondrial helicase /". Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-102-2/.
Testo completoBerg, Alonso Laetitia. "Déficits de la chaîne respiratoire mitochondriale avec instabilité de l’ADN mitochondrial : identification de nouveaux gènes et mécanismes". Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2016. http://www.theses.fr/2016AZUR4101.
Testo completoNon communiqué
Weber, Katharina Karin. "Studies of mitochondrial DNA". Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295072.
Testo completoMyers, K. A. "Alkylation of mitochondrial DNA". Thesis, University of Manchester, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234216.
Testo completoJohansson, Jennie. "Epigenetic Regulation of Mitochondrial DNA". Thesis, Linköpings universitet, Institutionen för fysik, kemi och biologi, 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-166684.
Testo completoWertzler, Kelsey Janel. "High mobility group A1 and mitochondrial transcription factor A compete for binding to mitochondrial DNA". Pullman, Wash. : Washington State University, 2009. http://www.dissertations.wsu.edu/Thesis/Summer2009/k_wertzler_051409.pdf.
Testo completoTitle from PDF title page (viewed on July 21, 2009). "School of Molecular Biosciences." Includes bibliographical references.
Gu, Mei. "Mitochondrial function in Parkinson's disease and other neurodegenerative diseases". Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322371.
Testo completoHastings, Patsy-Ann Susan. "MITOCHONDRIAL DNA ANALYSIS BY PYROSEQUENCING". Master's thesis, University of Central Florida, 2004. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/4447.
Testo completoM.S.
Department of Chemistry
Arts and Sciences
Chemistry
Williams, Andrew. "Functional and molecular analysis of defects of the mitochondrial respiratory chain". Thesis, The University of Sydney, 1998. https://hdl.handle.net/2123/27688.
Testo completoLogan, Angela. "Production of reactive oxygen species in mitochondria and mitochondrial DNA damage". Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609201.
Testo completoMarrouf, Nedal. "Mitochondrial DNA in atrial fibrillation". Thesis, St George's, University of London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415671.
Testo completoKing, Louise. "Mitophagy and mitochondrial DNA disease". Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10043560/.
Testo completoCraig, Elaine. "Protein import into cardiac mitochondria". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ39261.pdf.
Testo completoBrierley, Elizabeth Jane. "Defects of mitochondrial DNA and mitochondrial energy production in ageing". Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323477.
Testo completoKollberg, Gittan. "Crisis in energy metabolism : mitochondrial defects and a new disease entity /". Göteborg : Department of Pathology, Institute of Biomedicine, The Sahlgrenska Academy at Göteborg University, 2007. http://hdl.handle.net/2077/779.
Testo completoPeeva, Viktoriya [Verfasser]. "Rearranged DNA in mitochondrial DNA maintenance disorders / Viktoriya Peeva". Bonn : Universitäts- und Landesbibliothek Bonn, 2015. http://d-nb.info/1077289669/34.
Testo completoBendall, Kate E. "Inheritance of mitochondrial mutations". Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320141.
Testo completoIbrahim, Noha. "Physiological mechanisms underlying DNA import into mitochondria and prospects for mitochondrial transfection". Université Louis Pasteur (Strasbourg) (1971-2008), 2008. http://www.theses.fr/2008STR13051.
Testo completoThere are considerable gaps in the understanding of the mitochondrial genetic systems and dysfunctions related to mutations in the mitochondrial DNA cannot be complemented. This is mainly due to the fact that conventional transformation of mitochondria has been unsuccessful for plants and mammals and is currently possible only for the yeast Saccharomyces cerevisiae and the green alga Chlamydomonas reinhardtii. No gene therapy strategy has thus been developed for genetic diseases due to mitochondrial DNA mutations. However, in collaboration with the groups of Y. Konstantinov (Irkutsk, Russia) and R. N. Lightowlers (Newcastle, UK), our laboratory has shown that isolated plant [1], mammalian [2] and yeast mitochondria have a natural potential to incorporate, repair and express foreign DNA. To understand, optimize and potentially use this process for mitochondrial transfection in vivo, I studied the import mechanism through biochemical, physiological and proteomic approaches. Some genetic analyses using yeast mutants were run in parallel in our laboratory. The voltage-dependent anion channel (VDAC) was identified as the putative translocator through the outer membrane. In the case of plant mitochondria, DNA import seems to follow nucleotide transport pathways to cross the inner membrane and to be concomitant with phosphate uptake and proton exchange. Nucleotide carriers also seem to play a role in DNA translocation into yeast organelles. Effectors and inhibitors have a limited effect on DNA transport into mammalian mitochondria, so that it is still difficult to figure out how the DNA crosses the inner membrane in this case. To directly identify the import complex, we designed DNA substrates with a bulky end which get stuck in the membranes during translocation. Using this system, we proved that mitochondrial protein import is not influenced when the DNA import channel is blocked, indicating that the two pathways do not overlap. On the contrary, it seems that DNA import might have some step(s) in common with another natural mitochondrial transport process: the import of cytosolic transfer RNAs (tRNAs) which compensates for the lack of a number of tRNA genes in plant organelle genomes [3]. To further characterise DNA translocation through the outer membrane and look for putative "receptors", we have analysed cyanine labeling of intact plant mitochondria in DNA import conditions. Proteins masked by the DNA were subsequently identified by mass spectrometry. However, cyanines turned out to be able to cross the outer membrane and label proteins accessible in the intermembrane space. Differential labeling nevertheless highlighted again the VDAC isoforms and two potential "receptor" candidates: the precursor of the ATP synthase beta subunit, which is present on the outer membrane, and a complex I subunit of unknown function. Mitochondrial transformation will need the maintenance of the imported DNA in the organelles. We showed that uracil-containing DNA imported into plant mitochondria can be specifically repaired in organello through a base excision repair mechanism. The first step in such a pathway is carried out by a DNA glycosylase. Through in vivo and in vitro assays, we demonstrated that uracil DNA glycosylase and 8-oxo guanine DNA glycosylase are indeed targeted to mitochondria in plants. A "rolling circle" replication pathway is likely to exist in plant mitochondria and might enable to maintain a properly designed DNA sequence upon import. However, this will require circular DNA, whereas only linear DNA is a substrate for import. We have thus analysed the in organello circularization of a linear DNA imported into plant mitochondria. Concerning the in vivo relevance of the DNA import process, we have hypothesized that it might be the basis for paternal transmission of an 11. 6 kb mitochondrial plasmid in Brassica napus [4]. We showed that this plasmid is indeed efficiently imported into isolated Brassica mitochondria. The import efficiency is due to the inverted repeats present at the ends of the plasmid and these sequences will be included in custom substrates for in vivo assays. To progress towards mitochondrial transformation in vivo, we started a new approach using DQAsomes as potential intracellular vehicles [5]. These vesicles have the property of binding DNA. They can cross the plasma membrane of mammalian cells and subsequently show a mitochondrial tropism. When contacting mitochondria, they release their DNA cargo [5], which we expect then to be imported into the organellles through the mechanism that we have studied in vitro. So far, my experiments show that DNA presented to isolated plant mitochondria by DQAsomes is imported. In vivo mitochondrial transfection assays will now be developed on this basis in plant and human cells using reporter constructs
Yu, Emma Pei Kuen. "Mitochondrial DNA damage, dysfunction and atherosclerosis". Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648537.
Testo completoSwalwell, Helen. "Mitochondrial DNA Mutations in Human Disease". Thesis, University of Newcastle upon Tyne, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.485565.
Testo completoNilsson, Martina. "Mitochondrial DNA in Sensitive Forensic Analysis". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7458.
Testo completoMcVeigh, Helen Patricia. "Mitochondrial DNA and salmonid population structure". Thesis, Queen's University Belfast, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.352951.
Testo completoElliott, Hannah. "Epidemiology of mitochondrial DNA point mutations". Thesis, University of Newcastle Upon Tyne, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442343.
Testo completoClark, Kim Michelle. "Mitochondrial DNA disease : pathogenesis and treatment". Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262993.
Testo completoIves, Daniel Jeremy. "Unravelling biased segregation of mitochondrial DNA". Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648336.
Testo completoBowmaker, Mark Richard. "Replication of the mouse mitochondrial DNA". Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614689.
Testo completoHine, Donna Louise. "Mitochondrial DNA depletion and insulin secretion". Thesis, University of Newcastle upon Tyne, 2013. http://hdl.handle.net/10443/1906.
Testo completoSchubert, Susanne, Sandra Heller, Birgit Löffler, Ingo Schäfer, Martina Seibel, Gaetano Villani e Peter Seibel. "Generation of rho zero cells". Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-167888.
Testo completoFaccenda, Danilo. "The role of the ATPase inhibitory factor 1 (IF1) in the regulation of apoptotic cell death". Thesis, Royal Veterinary College (University of London), 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701678.
Testo completoVermulst, Marc. "Untangling mitochondrial mutagenesis and aging in mice /". Thesis, Connect to this title online; UW restricted, 2008. http://hdl.handle.net/1773/6321.
Testo completoCzajka, Anna Natalia. "Hyperglycaemia-induced mitochondrial DNA changes and mitochondrial dysfunction in diabetic nephropathy". Thesis, King's College London (University of London), 2015. https://kclpure.kcl.ac.uk/portal/en/theses/hyperglycaemiainduced-mitochondrial-dna-changes-and-mitochondrial-dysfunction-in-diabetic-nephropathy(915dd388-e5d2-4b2e-a317-bbd9a7ddb14d).html.
Testo completoXu, Xiufeng. "Studies of mammalian mitochondrial genomes with special emphasis on the perissodactyla". Lund : Lund University, 1996. http://catalog.hathitrust.org/api/volumes/oclc/38161173.html.
Testo completoMeagher, Martin. "Role of tyrosyl-DNA-phosphodiesterase I in mitochondrial DNA repair". Thesis, University of Newcastle upon Tyne, 2013. http://hdl.handle.net/10443/1940.
Testo completoGaspari, Martina. "Molecular mechanisms for transcription in mammalian mitochondria /". Stockholm : Karolinska institutet, 2006. http://diss.kib.ki.se/2006/91-7357-012-5/.
Testo completoCailloce, Justine. "Identification des facteurs de reconnaissance des mitochondries spermatiques dans l’embryon de C. elegans, garants de l’hérédité mitochondriale uni-parentale maternelle". Electronic Thesis or Diss., Sorbonne université, 2023. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2023SORUS497.pdf.
Testo completoMitochondria are essential cellular components, found in the cytoplasm of the vast majority of cells in eukaryotic organisms. They are involved in a number of mechanisms that ensure proper cell function, such as apoptosis and calcium storage. The main mitochondrial function is carried out by the inner mitochondrial membrane, where protein complexes are located, enabling the production of adenosine triphosphate or ATP, the energy source for our cells. In the animal kingdom, mitochondria are the only organelles other than the nucleus to possess a genome, the mitochondrial DNA or mtDNA. The 37 genes carried by this mitochondrial genome represent only a small proportion of a cell's genes, but they are vital nevertheless. Indeed, all the proteins encoded by the mitochondrial genome are required for energy production. Therefore, disturbances in mitochondria composition and function, caused by various mutations, have been shown to be deleterious and the source of many pathologies with a wide range of symptoms.During my thesis, I focused on an atypical aspect of these organelles: their mode of inheritance. Indeed, while nuclear DNA is inherited in equal parts from each parent, the mitochondrial DNA is inherited exclusively from the mother. This particular mode of inheritance is known as maternal uni-parental mitochondrial transmission. This event of sexual reproduction is highly conserved throughout evolution, suggesting its major interest for different animal and plant species, even though some exceptions exist. This maternal uniparental inheritance results from the active degradation by an autophagy dependent mechanism, of paternal mitochondria, which enter the oocyte cytoplasm during fertilization. However, the reasons for this mode of inheritance and the mechanisms regulating it are not fully understood. For my research, I used the model organism C. elegans, which also exhibits maternal uni-parental mitochondrial inheritance. Taking advantage of the experimental advantages of this model system, my particular aim was to identify the markers carried by sperm mitochondria which trigger their recognition in the oocyte. As a first step, using imaging and a candidate gene approach, I assessed the role of poly-ubiquitylation marks in the targeting of sperm mitochondria in the embryo. The lack of a clear role for poly-ubiquitylation led me to develop a comprehensive and unbiased proteomic approach to identify mitochondrial recognition factors. This method of indirect proximity labeling by biotinylation enabled me to identify in the early C. elegans embryo, the interactome of a major protein controlling the autophagy machinery. From this interactome, I then drew up a list of candidate proteins that could act as degradation signals for the degradation of sperm mitochondria in the early embryo of C. elegans. Finally, I took part in the team's common work to establish a model of biparental heredity. To this end, we are combining all existing mutants known to act in the sperm mitochondria degradation, as well as in somatic mitophagy processes. Establishing such a genotype highlights the complexity of the mechanisms involved in uniparental inheritance, some of which remain to be elucidated
Bris, Céline. "Influence de la génétique mitochondriale en pathologie : apport des techniques de séquençage haut débit Deep sequencing shows that oocytes are not prone to accumulate mtDNA heteroplasmic mutations during ovarian ageing Novel NDUFS4 gene mutation in an atypical late-onset mitochondrial form of multifocal dystonia". Thesis, Angers, 2017. http://www.theses.fr/2017ANGE0093.
Testo completoMitochondrial diseases are common metabolic disorders characterized by strong clinical and genetic heterogeneity, in particular due to the dependence on 2 genomes, nuclear (nDNA) and mitochondrial DNA (mtDNA), and the concept of mitochondrial heteroplasmy. The purpose of this work was to develop a strategy for the analysis of the mtDNA through next-generation sequencing (NGS), and then to apply it to the study of mitochondrial diseases and those related to aging: primary open-angle glaucoma (POAG) and ovarian aging. After validating the performances of our NGS strategy for the detection and quantification of mtDNA variations, we confirmed the power of systematic analysis of the whole mitochondrial genome with the use of uroepithelial cells for mitochondrial diseases diagnosis and the identification of novel mtDNA variants. However, these advances generate new challenges such as the interpretation of low percentages of mtDNA mutations or the prediction of the pathogenicity of new variants. For aging-related diseases, we have identified the possible protective role of the mitochondrial haplogroups T and H in women, respectively in the occurrence and severity of POAG, suggesting that mtDNA influence is drivenby gender, and thus the importance of gender stratification for association studies. By contrast, we did not observe any accumulation of mtDNA abnormalities in early ovarian aging. In perspective, we report the identification of a nDNA mutation in an atypical phenotype, highlighting the complexity of mitochondrial diseases diagnosis, due to this double genome
Heupink, Tim Hermanus. "Avian Mitochondrial DNA and Microevolution across Biological Organisation". Thesis, Griffith University, 2013. http://hdl.handle.net/10072/366002.
Testo completoThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Griffith School of Environment
Science, Environment, Engineering and Technology
Full Text
Hill, Catherine E. "Mitochondrial DNA variation in Island Southeast Asia". Thesis, University of Huddersfield, 2005. http://eprints.hud.ac.uk/id/eprint/22331/.
Testo completoStringer, Henry. "Mitochondrial DNA alterations and statin-induced myopathy". Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/9949.
Testo completoMahrous, Enas. "Regulation of mitochondrial DNA accumulation during oogenesis". Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97087.
Testo completoDurant sa croissance, chaque ovocyte doit accumuler un grand nombre de mitochondries, essentielles pour le développement embryonnaire ultérieur. Après la fécondation, le stock de mitochondries ovocytaire doit être suffisant pour assurer les divisions successives de chaque blastomère de lèmbryon puisque que la reprise de la réplication de làDN mitochondrial (mtDN ne s`observe quàvant l`implantation. Les mécanismes régulant làccumulation de mtDNA durant la croissance ovocytaire et les étapes de celle-ci sont cependant encore mal connus. Dans ce travail, nous avons mis au point une technique PCR permettant de mesurer la quantité de mtDNA dans un seul ovocyte. Les résultats montrent que la quantité de mtDNA augmente progressivement pendant la croissance ovocytaire pour atteindre environ 175000 copies par cellule. Lorsque l`ovocyte atteint sa taille finale, làccumulation de mtDNA sàrrête, suggérant une corrélation entre la croissance et làccumulation de mtDNA. Nous avons ensuite vérifié cette hypothèse en mesurant la quantité de mtDNA pendant la croissance ovocytaire in vitro dans différentes conditions. De la même manière, nous avons observé une accumulation de mtDNA durant la croissance ovocytaire in vitro. Cependant, bien que la croissance ovocytaire soit moindre in vitro comparée à celle obtenue in vivo, la quantité de mtDNA accumulée est comparable dans les deux conditions. Lorsque les ovocytes sont mis en culture en présence dùn inhibiteur de la phosphoinosotide-3 kinase (LY294002), ou en làbsence de cellule de la granulosa, la croissance ovocytaire in vitro est inhibée mais làccumulation de mtDNA est maintenue. Ces résultats montrent que làccumulation de mtDNA est indépendante de la croissance ovocytaire. Nous avons ensuite analysé lèxpression des gènes nucléaires essentiels à la réplication de mtDNA. Lèxpression des ARNm de Tfam, Polga, et Polgb augmente parallèlement à la croissance ovocytaire mais diminue lorsque l`ovocyte a atteint sa taille finale. Ces résultats suggèrent que làrrêt de làccumulation de mtDNA en fin de croissance ovocytaire est liée à làrrêt de la transcription des gènes essentiels à sa réplication. La présence dàRNm de ces différents gènes pourraient être le facteur limitant la régulation de làccumulation de mtDNA dans l`ovocyte durant sa croissance. Nous avons également évalué la quantité dàTP dans les ovocytes. Les ovocytes en croissance sont plus riches en ATP que les ovocytes ayant atteints leur taille définitive et la quantité dàTP chute lors de la maturation méiotique de l`ovocyte. Ces résultats suggèrent que les ovocytes en croissance ont un besoin énergétique supérieur comparé á ceux á des stades ultérieurs.
Freeman, Emmerson Clare. "Molecular analysis of mutant human mitochondrial DNA". Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297942.
Testo completoMennuni, M. "Manipulating the segregation of human mitochondrial DNA". Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10047179/.
Testo completoCluett, Tricia Joy. "The mechanism of mammalian mitochondrial DNA replication". Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611167.
Testo completoGranycome, Caroline Louise. "Maintenance and segregation of human mitochondrial DNA". Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612947.
Testo completoDickinson, Adam. "The role of mitochondrial DNA in tumorigenesis". Thesis, University of Warwick, 2013. http://wrap.warwick.ac.uk/58415/.
Testo completoBrennan, Rebecca Ruth. "Genetic factors modulating mitochondrial DNA copy number". Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3960.
Testo completo