Relevant bibliographies by topics / Mitochondria. DNA

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Academic literature on the topic 'Mitochondria. DNA'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Mitochondria. DNA"

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Basu, Urmimala, Alicia M. Bostwick, Kalyan Das, Kristin E. Dittenhafer-Reed, and Smita S. Patel. "Structure, mechanism, and regulation of mitochondrial DNA transcription initiation." Journal of Biological Chemistry 295, no. 52 (October 30, 2020): 18406–25. http://dx.doi.org/10.1074/jbc.rev120.011202.

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Mitochondria are specialized compartments that produce requisite ATP to fuel cellular functions and serve as centers of metabolite processing, cellular signaling, and apoptosis. To accomplish these roles, mitochondria rely on the genetic information in their small genome (mitochondrial DNA) and the nucleus. A growing appreciation for mitochondria's role in a myriad of human diseases, including inherited genetic disorders, degenerative diseases, inflammation, and cancer, has fueled the study of biochemical mechanisms that control mitochondrial function. The mitochondrial transcriptional machinery is different from nuclear machinery. The in vitro re-constituted transcriptional complexes of Saccharomyces cerevisiae (yeast) and humans, aided with high-resolution structures and biochemical characterizations, have provided a deeper understanding of the mechanism and regulation of mitochondrial DNA transcription. In this review, we will discuss recent advances in the structure and mechanism of mitochondrial transcription initiation. We will follow up with recent discoveries and formative findings regarding the regulatory events that control mitochondrial DNA transcription, focusing on those involved in cross-talk between the mitochondria and nucleus.
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Varma, V. A., C. M. Cerjan, K. L. Abbott, and S. B. Hunter. "Non-isotopic in situ hybridization method for mitochondria in oncocytes." Journal of Histochemistry & Cytochemistry 42, no. 2 (February 1994): 273–76. http://dx.doi.org/10.1177/42.2.8288868.

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We used in situ hybridization to specifically identify mitochondria in a series of formalin-fixed, paraffin-embedded oncocytic lesions. Digoxigenin-labeled DNA probes were generated by the polymerase chain reaction (PCR), with primers designed to amplify a mitochondrion-specific 154 BP sequence within the ND4 coding region. Probes were hybridized with mitochondrial DNA under stringent conditions. Oncocytes were strongly and consistently stained, reflecting the high copy number of mitochondrial DNA within these cells. Because of the presence of endogenous biotin within mitochondria, digoxigenin is preferable to biotin as a label for detection of mitochondria.
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Valdés-Aguayo, José J., Idalia Garza-Veloz, José I. Badillo-Almaráz, Sofia Bernal-Silva, Maria C. Martínez-Vázquez, Vladimir Juárez-Alcalá, José R. Vargas-Rodríguez, et al. "Mitochondria and Mitochondrial DNA: Key Elements in the Pathogenesis and Exacerbation of the Inflammatory State Caused by COVID-19." Medicina 57, no. 9 (September 3, 2021): 928. http://dx.doi.org/10.3390/medicina57090928.

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Background and Objectives. The importance of mitochondria in inflammatory pathologies, besides providing energy, is associated with the release of mitochondrial damage products, such as mitochondrial DNA (mt-DNA), which may perpetuate inflammation. In this review, we aimed to show the importance of mitochondria, as organelles that produce energy and intervene in multiple pathologies, focusing mainly in COVID-19 and using multiple molecular mechanisms that allow for the replication and maintenance of the viral genome, leading to the exacerbation and spread of the inflammatory response. The evidence suggests that mitochondria are implicated in the replication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which forms double-membrane vesicles and evades detection by the cell defense system. These mitochondrion-hijacking vesicles damage the integrity of the mitochondrion’s membrane, releasing mt-DNA into circulation and triggering the activation of innate immunity, which may contribute to an exacerbation of the pro-inflammatory state. Conclusions. While mitochondrial dysfunction in COVID-19 continues to be studied, the use of mt-DNA as an indicator of prognosis and severity is a potential area yet to be explored.
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Baysal, Bora. "Mitochondria: More than Mitochondrial DNA in Cancer." PLoS Medicine 3, no. 3 (March 28, 2006): e156. http://dx.doi.org/10.1371/journal.pmed.0030156.

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Faria, Rúben, Eric Vivés, Prisca Boisguerin, Angela Sousa, and Diana Costa. "Development of Peptide-Based Nanoparticles for Mitochondrial Plasmid DNA Delivery." Polymers 13, no. 11 (June 1, 2021): 1836. http://dx.doi.org/10.3390/polym13111836.

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A mitochondrion is a cellular organelle able to produce cellular energy in the form of adenosine triphosphate (ATP). As in the nucleus, mitochondria contain their own genome: the mitochondrial DNA (mtDNA). This genome is particularly susceptible to mutations that are at the basis of a multitude of disorders, especially those affecting the heart, the central nervous system and muscles. Conventional clinical practice applied to mitochondrial diseases is very limited and ineffective; a clear need for innovative therapies is demonstrated. Gene therapy seems to be a promising approach. The use of mitochondrial DNA as a therapeutic, optimized by peptide-based complexes with mitochondrial targeting, can be seen as a powerful tool in the reestablishment of normal mitochondrial function. In line with this requirement, in this work and for the first time, a mitochondrial-targeting sequence (MTS) has been incorporated into previously researched peptides, to confer on them a targeting ability. These peptides were then considered to complex a plasmid DNA (pDNA) which contains the mitochondrial gene ND1 (mitochondrially encoded NADH dehydrogenase 1 protein), aiming at the formation of peptide-based nanoparticles. Currently, the ND1 plasmid is one of the most advanced bioengineered vectors for conducting research on mitochondrial gene expression. The formed complexes were characterized in terms of pDNA complexation capacity, morphology, size, surface charge and cytotoxic profile. These data revealed that the developed carriers possess suitable properties for pDNA delivery. Furthermore, in vitro studies illustrated the mitochondrial targeting ability of the novel peptide/pDNA complexes. A comparison between the different complexes revealed the most promising ones that complex pDNA and target mitochondria. This may contribute to the optimization of peptide-based non-viral systems to target mitochondria, instigating progress in mitochondrial gene therapy.
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Bertrand, Helmut. "Senescence is coupled to induction of an oxidative phosphorylation stress response by mitochondrial DNA mutations in Neurospora." Canadian Journal of Botany 73, S1 (December 31, 1995): 198–204. http://dx.doi.org/10.1139/b95-246.

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In Neurospora and other genera of filamentous fungi, the occurrence of a mutation affecting one or several genes on the chromosome of a single mitochondrion can trigger the gradual displacement of wild-type mitochondrial DNA by mutant molecules in asexually propagated cultures. As this displacement progresses, the cultures senesce gradually and die if the mitochondrial mutation is lethal, or develop respiratory deficiencies if the mutation is nonlethal. Mitochondrial mutations that elicit the displacement of wild-type mitochondrial DNAs are said to be "suppressive." In the strictly aerobic fungi, suppressiveness appears to be associated exclusively with mutations that diminish cytochrome-mediated mitochondrial redox functions and, thus, curtail oxidative phosphorylation. In Neurospora, suppressiveness is connected to a regulatory system through which cells respond to chemical or genetic insults to the mitochondrial electron-transport system by increasing the number of mitochondria approximately threefold. Mutant alleles of two nuclear genes, osr-1 and osr-2, affect this stress response and abrogate the suppressiveness of mitochondrial mutations. Therefore, we propose that mitochondrial mutations are suppressive because their phenotypic effect is limited to the organelles within which the mutant DNA is located. Consequently, mitochondria that are "homozygous" for a mutant allele are functionally crippled and are induced to proliferate more rapidly than the normal mitochondria with which they coexist in a common protoplasm. While this model provides a plausible explanation for the suppressiveness of mitochondrial mutations in the strictly aerobic fungi, it may not account for the biased transmission of mutant mitochondrial DNAs in the facultatively anaerobic yeasts. Key words: mitochondria, mitochondrial DNA, mutations, suppressiveness, oxidative phosphorylation, stress response.
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Schapira, Anthony. "Mitochondrial DNA and disease: What happens when things go wrong." Biochemist 27, no. 3 (June 1, 2005): 24–27. http://dx.doi.org/10.1042/bio02703024.

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Mitochondria are ubiquitous in eukaryotic cells and one of their important functions is to provide ATP via oxidative phosphorylation (OXPHOS). The mitochondria also host other biochemical pathways, including -oxidation, Krebs' citric acid cycle and parts of the urea cycle. Thus, the mitochondria play a pivotal role in cellular biochemistry. The relationship of mitochondria to human disease has been identified only recently, but has now become one of the most rapidly expanding areas of human pathology. Mitochondrial disorders may be a consequence of inherited defects of either the nuclear or mitochondrial genomes or, alternatively, may be due to endogenous or exogenous environmental toxins. This article will focus upon abnormalities of mitochondrial DNA (mtDNA) and human disease.
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Almannai, Mohammed, Ayman W. El-Hattab, and Fernando Scaglia. "Mitochondrial DNA replication: clinical syndromes." Essays in Biochemistry 62, no. 3 (June 27, 2018): 297–308. http://dx.doi.org/10.1042/ebc20170101.

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Each nucleated cell contains several hundreds of mitochondria, which are unique organelles in being under dual genome control. The mitochondria contain their own DNA, the mtDNA, but most of mitochondrial proteins are encoded by nuclear genes, including all the proteins required for replication, transcription, and repair of mtDNA. MtDNA replication is a continuous process that requires coordinated action of several enzymes that are part of the mtDNA replisome. It also requires constant supply of deoxyribonucleotide triphosphates(dNTPs) and interaction with other mitochondria for mixing and unifying the mitochondrial compartment. MtDNA maintenance defects are a growing list of disorders caused by defects in nuclear genes involved in different aspects of mtDNA replication. As a result of defects in these genes, mtDNA depletion and/or multiple mtDNA deletions develop in affected tissues resulting in variable manifestations that range from adult-onset mild disease to lethal presentation early in life.
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Bradshaw, Patrick C., and David C. Samuels. "A computational model of mitochondrial deoxynucleotide metabolism and DNA replication." American Journal of Physiology-Cell Physiology 288, no. 5 (May 2005): C989—C1002. http://dx.doi.org/10.1152/ajpcell.00530.2004.

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We present a computational model of mitochondrial deoxynucleotide metabolism and mitochondrial DNA (mtDNA) synthesis. The model includes the transport of deoxynucleosides and deoxynucleotides into the mitochondrial matrix space, as well as their phosphorylation and polymerization into mtDNA. Different simulated cell types (cancer, rapidly dividing, slowly dividing, and postmitotic cells) are represented in this model by different cytoplasmic deoxynucleotide concentrations. We calculated the changes in deoxynucleotide concentrations within the mitochondrion during the course of a mtDNA replication event and the time required for mtDNA replication in the different cell types. On the basis of the model, we define three steady states of mitochondrial deoxynucleotide metabolism: the phosphorylating state (the net import of deoxynucleosides and export of phosphorylated deoxynucleotides), the desphosphorylating state (the reverse of the phosphorylating state), and the efficient state (the net import of both deoxynucleosides and deoxynucleotides). We present five testable hypotheses based on this simulation. First, the deoxynucleotide pools within a mitochondrion are sufficient to support only a small fraction of even a single mtDNA replication event. Second, the mtDNA replication time in postmitotic cells is much longer than that in rapidly dividing cells. Third, mitochondria in dividing cells are net sinks of cytoplasmic deoxynucleotides, while mitochondria in postmitotic cells are net sources. Fourth, the deoxynucleotide carrier exerts the most control over the mtDNA replication rate in rapidly dividing cells, but in postmitotic cells, the NDPK and TK2 enzymes have the most control. Fifth, following from the previous hypothesis, rapidly dividing cells derive almost all of their mtDNA precursors from the cytoplasmic deoxynucleotides, not from phosphorylation within the mitochondrion.
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Wang, Sheng-Fan, Shiuan Chen, Ling-Ming Tseng, and Hsin-Chen Lee. "Role of the mitochondrial stress response in human cancer progression." Experimental Biology and Medicine 245, no. 10 (April 23, 2020): 861–78. http://dx.doi.org/10.1177/1535370220920558.

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Mitochondria are important organelles that are responsible for cellular energy metabolism, cellular redox/calcium homeostasis, and cell death regulation in mammalian cells. Mitochondrial dysfunction is involved in various diseases, such as neurodegenerative diseases, cardiovascular diseases, immune disorders, and cancer. Defective mitochondria and metabolism remodeling are common characteristics in cancer cells. Several factors, such as mitochondrial DNA copy number changes, mitochondrial DNA mutations, mitochondrial enzyme defects, and mitochondrial dynamic changes, may contribute to mitochondrial dysfunction in cancer cells. Some lines of evidence have shown that mitochondrial dysfunction may promote cancer progression. Here, several mitochondrial stress responses, including the mitochondrial unfolded protein response and the integrated stress response, and several mitochondrion-derived molecules (reactive oxygen species, calcium, oncometabolites, and others) are reviewed; these pathways and molecules are considered to act as retrograde signaling regulators in the development and progression of cancer. Targeting these components of the mitochondrial stress response may be an important strategy for cancer treatment. Impact statement Dysregulated mitochondria often occurred in cancers. Mitochondrial dysfunction might contribute to cancer progression. We reviewed several mitochondrial stresses in cancers. Mitochondrial stress responses might contribute to cancer progression. Several mitochondrion-derived molecules (ROS, Ca2+, oncometabolites, exported mtDNA, mitochondrial double-stranded RNA, humanin, and MOTS-c), integrated stress response, and mitochondrial unfolded protein response act as retrograde signaling pathways and might be critical in the development and progression of cancer. Targeting these mitochondrial stress responses may be an important strategy for cancer treatment.
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Dissertations / Theses on the topic "Mitochondria. DNA"

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Rebelo, Adriana. "Probing Mitochondrial DNA Structure with Mitochondria-Targeted DNA Methyltransferases." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/344.

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The mitochondria contain their own genome, which is organized in a dynamic high-order nucleoid structure consisting of several copies of mitochondrial DNA (mtDNA) molecules associated with proteins. The mitochondrial nucleoids are the units of mtDNA inheritance, and are the sites of mtDNA transcription, replication and maintenance. Therefore, the integrity of mitochondrial nucleoids is a key determinant of mitochondrial metabolism and the bioenergetic state of the cell. Deciphering the interaction of mtDNA with proteins in nucleoprotein complexes is fundamental to understand the mechanisms of mtDNA segregation leading to mitochondrial dysfunction and to develop therapies to treat diseases associated with mtDNA mutations. The work presented in this dissertation provides essential insights into the dynamics of mtDNA interaction with nucleoid proteins. In order to unveil the organization of the mitochondrial genome, we have mapped major regulatory regions of the mtDNA in vivo using mitochondrial-targeted DNA methyltransferases. In chapter 2, we have demonstrated that DNA methyltranferases are powerful tools in probing mtDNA-protein interactions in living cells. The DNA methyltransferases' accessibility to their cognate sites in the mtDNA is negatively correlated with the frequency and binding strength that protein factors occupy a specific site. Our results show that the transcription termination region (TERM) within the tRNALeu(UUR) gene is consistently and strongly protected from methylation, suggesting frequent and high affinity binding of mTERF1 (mitochondrial transcription termination factor 1). DNA methyltransferases have also been shown to be effective in detecting changes in mitochondrial nucleoid architecture due to nucleoid remodeling. We were able to determine changes in the packaging state of mitochondrial nucleoids by monitoring changes in mtDNA accessibility. The impact of altered levels of major nucleoid proteins was assessed by monitoring changes in mtDNA methylation pattern. We observed a more condensed nucleoid state causing a decrease in mtDNA methylation when the levels of the mitochondrial transcription factor A (TFAM) were altered. Changes in mtDNA methylation pattern were also evident when cells were treated with ethidium bromide (EtBr) and hydrogen peroxide. The mtDNA nucleoids adopted a less compact state during rapid mtDNA replication after EtBr treatment. In contrast, we observed a more compact mtDNA, less accessible to DNA methyltransferase after hydrogen peroxide treatment. Our results indicate that mitochondrial nucleoids are not static, but are constantly been modulated in response to factors that affect the nucleoid environment. In chapter 3, we identified the in vivo DNA binding sites of major transcription regulatory proteins, TFAM and mTERF3 using a targeted gene methylation (TAGM) strategy. In this approach, the mtDNA binding protein is fused to a DNA methyltransferase as an attempt to selectively methylate the sites adjacent to the protein target DNA region. Knowledge on how proteins interact with the mtDNA in high-order structures, which function as a mitochondrial genetic unit, will help elucidate the segregation and accumulation of mutated mtDNA in diseased tissues.
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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.

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Le plasma transporte des cellules sanguines avec un mélange de composés, y compris les nutriments, déchets, anticorps, et messagers chimiques... dans tout l'organisme. Des facteurs non solubles tels que l’ADN circulant et les vésicules extracellulaires ont récemment été ajoutés à la liste de ces composants et ont fait l'objet d'études approfondies en raison de leur rôle dans la communication intercellulaire. Or, l’ADN circulant (ADNcir) est composé de fragments d’ADN libres ou associés à d’autres particules, libérés par tous les types cellulaires. Cet ADN est non seulement de l'ADN génomique mais aussi de l'ADN mitochondrial extra-chromosomique. De nombreux travaux réalisés au cours des dernières années indiquent que l’analyse quantitative et qualitative de l’ADNcir représente une avancée dans les applications cliniques en tant que biomarqueur non invasif de diagnostic, de pronostic et de suivi thérapeutique. Cependant, malgré l'avenir prometteur de cet ADNcir dans les applications cliniques, notamment en oncologie, les connaissances sur ses origines, sa composition et ses fonctions qui pourraient pourtant permettre d’optimiser considérablement sa valeur diagnostique, font encore défaut. Le principal objectif de ma thèse a été d’identifier et de caractériser les propriétés structurales de l’ADN extracellulaire d’origine mitochondrial. En examinant l'intégrité de cet ADN, ainsi que la taille et la densité des structures associées, ce travail a révélé la présence de particules denses d’une taille supérieure à 0,2 µm contenant des génomes mitochondriaux complets et non fragmentés. Nous avons caractérisé ces structures notamment par microscopie électronique et cytométrie en flux et nous avons identifié des mitochondries intactes dans le milieu extracellulaire in vitro et ex-vivo (dans des échantillons de plasma d’individus sains). Une consommation d'oxygène par ces mitochondries a été détectée par la technique du Seahorse, suggérant qu'au moins une partie de ces mitochondries extracellulaires intactes pourraient être fonctionnelles. Par ailleurs, j’ai participé à d’autres travaux réalisées dans l’équipe, dont (1) une étude visant à évaluer l’influence des paramètres pré-analytiques et démographiques sur la quantification d’ADNcir d’origine nucléaire et mitochondrial sur une cohorte composée de 104 individus sains et 118 patients atteints de cancer colorectal métastatique, (2) une étude dont l’objectif était d’évaluer l’influence de l’hypoxie sur le relargage de l’ADN circulant in vitro et in vivo, et (3) une étude visant à évaluer le potentiel de l’analyse de l’ADN circulant dans le dépistage et la détection précoce du cancer. Ce manuscrit présente une synthèse récente de la littérature sur l’ADNcir, ses différents mécanismes de relargage, qui vont de pair avec la caractérisation structurelle de cet ADN, ses aspects fonctionnels et ses différentes applications en cliniques. De plus, cette thèse apporte des connaissances nouvelles sur la structure de l’ADN mitochondrial extracellulaire tout en ouvrant de nouvelles pistes de réflexion notamment sur l’impact que pourrait avoir la présence de ces structures circulantes sur la communication cellulaire, l’inflammation et des applications en clinique
Plasma 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
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Craig, 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.

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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/.

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Boyer, 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.

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Le génome mitochondrial est minimal et la plupart des protéines mitochondriales sont aujourd’hui codées par des gènes nucléaires. Ainsi, bien que les génomes mitochondriaux et nucléaires soient physiquement séparés, ils communiquent via des signaux antérogrades (noyau vers mitochondrie) et rétrogrades (mitochondrie vers noyau), permettant la coordination de la biogenèse mitochondriale avec les besoins énergétiques cellulaires. Ces besoins énergétiques sont cycliques le plus souvent, et les horloges circadiennes régulent de nombreux aspects de la biologie des mitochondries, dont les dynamiques de fusion et fission qui façonnent l’architecture du réseau mitochondrial. Dans les foies de souris, le réseau oscille entre un état fusionné (pendant le jour) et des structures fragmentées (pendant la nuit). Un réseau fusionné est généralement associé à une production d’ATP plus efficace, alors que la fragmentation est associée à des niveaux de ROS et de mitophagie élevés. En d’autres termes, la fission offre à l’ADN mitochondrial une possibilité de s’échapper de son organelle. Des expériences de complémentations en levure ont montré que l’ADN mitochondrial (mtDNA) était capable de s’échapper de la mitochondrie et d’entrer dans le noyau. Chez les cellules humaines (HeLa), le génome mitochondrial entier et intact a été détecté dans le noyau. L’analyse de l’évolution des numts (séquences mitochondriales insérées dans le noyau) a montré que le processus d’intégration de nouvelles séquences mitochondriales dans le génome nucléaire était encore en cours. De plus, de nombreux évènements somatiques de fusion entre ADN mitochondrial et nucléaire (simts) ont été détectés dans des cellules cancéreuses humaines - c’est-à-dire dans un contexte d’instabilité génomique et de rythmes circadiens perturbés. La mitophagie est a priori responsable de la production de vésicules dans le cytoplasme contenant de mtDNA et potentiellement absorbables par le noyau. Puisque les dynamiques du réseau mitochondrial et la mitophagie sont régulés par les horloges circadiennes, nous avons étudié l’accumulation d’ADN mitochondrial dans le compartiment nucléaire en fonction du temps circadien. Cette question a été adressée dans le foie de souris, un tissus mammifère différentié. Nos travaux montrent que l’accumulation d’ADN mitochondrial dans le noyau de foie de souris est régulée par l’horloge circadienne, et atteint son zénith à la fin de la nuit circadienne. Dans le noyau, l’ADN mitochondrial est plus hydroxy-méthylé que dans le cytoplasme. Aussi, nous avons montré que perturber les horloges circadiennes modifiait la phase et l’amplitude des dynamiques d’ADN mitochondrial nucléaire. De plus, l’accumulation d’ARN mitochondrial nucléaire est concomitante à celle d’ADN mitochondrial nucléaire dans la plupart des conditions, et qu’elle est sensible aux challenges nutritionnels. Il est probable que ces dynamiques soient engendrées par le remodelage circadienne du réseau mitochondrial. La présence accrue d’insertions d’ADN mitochondrial dans les génomes nucléaires des tissus cancéreux ou âgés, pour lesquels les horloges circadiennes sont souvent perturbées, est peut-être due à une perte de la régulation des dynamiques de remodelage du réseau mitochondrial
The 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
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Logan, 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.

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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.

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Ibrahim, 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.

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Les mitochondries assurent des fonctions vitales dans la production d’énergie, les processus d’oxydo-réduction et le métabolisme des cellules eucaryotes. Ces organites possèdent leur propre système génétique. Le vieillissement pourrait être lié à leur dysfonctionnement progressif et les mutations dans leur génome sont à l’origine de nombreuses maladies dégénératives actuellement incurables. Ces pathologies neuromusculaires, qui comprennent par exemple les syndromes MERRF ("myoclonus epilepsy with ragged-red fibers") et MELAS ("mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes"), peuvent être extrêmement invalidantes et laissent pour l’instant les cliniciens démunis. Chez les plantes, les mutations non létales de l’ADN mitochondrial (ADNmt) se traduisent principalement par la stérilité mâle cytoplasmique, qui est très utilisée en agronomie. La biogenèse des mitochondries nécessite l’import de mille à deux mille protéines codées par le génome nucléaire mais le système génétique mitochondrial doit fournir un certain nombre de polypeptides qui sont essentiels pour la survie de la cellule car ce sont des composants de la chaîne respiratoire. Le maintien, l’intégrité et l’expression efficace du génome mitochondrial sont donc fondamentaux pour les organismes eucaryotes. La compréhension du système génétique mitochondrial est cependant très parcellaire et ses dysfonctionnements pathologiques dus à des mutations dans l'ADNmt ne peuvent pas être complémentés. Ceci est dû dans une large mesure à l’impossibilité de transformer génétiquement les mitochondries des plantes et des mammifères par des méthodes conventionnelles de type biolistique. Il est donc primordial de développer de nouvelles approches permettant de modifier l’information et l’expression génétique dans les mitochondries. Seules les mitochondries de la levure Saccharomyces cerevisiae et de la microalgue Chlamydomonas reinhardtii peuvent être transformées à l’heure actuelle in vivo1,2. L’électroporation a permis d’introduire puis de transcrire de l’ADN dans des mitochondries isolées de trypanosomatides (Leishmania tarentolae et Trypanosoma brucei)3 et de blé (Triticum aestivum)4. L’incorporation d'ADN par électroporation a également été décrite pour les mitochondries de souris (Mus musculus)5. La transcription de l'ADN ainsi incorporé a été revendiquée6 mais reste controversée. L’utilisation de chimères entre l’ADN et un peptide d’adressage mitochondrial est à l’étude7. La transfection de mitochondries de souris isolées par conjugaison avec des bactéries a également été décrite8. Aucune de ces techniques artificielles n’a donné lieu au développement d’une stratégie de transformation des mitochondries dans les cellules animales ou végétales. Dans ce contexte, notre laboratoire a montré, en collaboration avec l’équipe de Yuri Konstantinov (Institut de Physiologie et de Biochimie des Plantes de Sibérie, Irkoutsk, Russie), que les mitochondries végétales isolées ont la capacité d'importer de façon active de l'ADN double brin et que l'ADN ainsi incorporé peut être transcrit dans les organelles9. L’import est indépendant de la séquence et l’ADN incorporé est stable dans les mitochondries. Le processus a depuis été établi avec des mitochondries isolées de différentes espèces végétales. Ces résultats ont mis en évidence un nouveau mécanisme de transport mitochondrial qui a les caractéristiques d’un phénomène physiologique. Une approche similaire a démontré l’import d’ADN dans les mitochondries isolées de la levure S. Cerevisiae. Dans ce contexte, notre laboratoire a montré, en collaboration avec l’équipe de Yuri Konstantinov (Institut de Physiologie et de Biochimie des Plantes de Sibérie, Irkoutsk, Russie), que les mitochondries végétales isolées ont la capacité d'importer de façon active de l'ADN double brin et que l'ADN ainsi incorporé peut être transcrit dans les organelles9. L’import est indépendant de la séquence et l’ADN incorporé est stable dans les mitochondries. Le processus a depuis été établi avec des mitochondries isolées de différentes espèces végétales. Ces résultats ont mis en évidence un nouveau mécanisme de transport mitochondrial qui a les caractéristiques d’un phénomène physiologique. Une approche similaire a démontré l’import d’ADN dans les mitochondries isolées de la levure S. Cerevisiae
There 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
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Gaspari, Martina. "Molecular mechanisms for transcription in mammalian mitochondria /." Stockholm : Karolinska institutet, 2006. http://diss.kib.ki.se/2006/91-7357-012-5/.

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Wertzler, 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.

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Thesis (M.S. in biochemistry)--Washington State University, August 2009.
Title from PDF title page (viewed on July 21, 2009). "School of Molecular Biosciences." Includes bibliographical references.
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Books on the topic "Mitochondria. DNA"

1

Mitochondria. 2nd ed. Hoboken, N.J: John Wiley & Sons, 2008.

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John, Justin C. St. Mitochondrial DNA, mitochondria, disease, and stem cells. New York: Humana Press, 2013.

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St. John, Justin C., ed. Mitochondrial DNA, Mitochondria, Disease and Stem Cells. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-101-1.

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Organelle genes and genomes. New York: Oxford University Press, 1994.

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Einfluss von Kern und Zytoplasma auf die Organisation und Expression mitochondrialer Gene bei Triticum, Triticale und Secale. Berlin: J. Cramer, 1991.

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Replikation des mobilen Introns (plDNA) in Mitochondrien von Podospora anserina: Mechanismus und Auswirkungen auf die Alterung des Pilzes. Berlin: J. Cramer, 1994.

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Hickerson, Michael J. Post-glacial population history and genetic structure of the northern clingfish (Gobbiesox maeandricus), revealed from mtDNA analysis. [Berlin: Springer-Verlag, 2001.

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Extrachromosomale in-vitro-Genetik bei Pilzen: Chondriom-Vektoren bei Hefen. Berlin: J. Cramer, 1986.

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Mitochondrial medicine. New York: Humana Press, 2015.

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Einfluss struktureller Umordnungen des Chondrioms auf die Seneszenz bei Podospora anserina. Berlin: J. Cramer, 1988.

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Book chapters on the topic "Mitochondria. DNA"

1

Shokolenko, Inna N., Susan P. Ledoux, and Glenn L. Wilson. "Mitochondrial DNA Damage and Repair." In Mitochondria, 323–47. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-69945-5_15.

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Yeung, Ka Yu, Adam Dickinson, and Justin C. St. John. "The Role of Mitochondrial DNA in Tumorigenesis." In Mitochondrial DNA, Mitochondria, Disease and Stem Cells, 119–55. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-101-1_6.

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Thyagarajan, Dominic. "Clinical Approach to the Diagnosis of Mitochondrial Disease." In Mitochondrial DNA, Mitochondria, Disease and Stem Cells, 1–23. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-101-1_1.

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McKenzie, Matthew. "Mitochondrial DNA Mutations and Their Effects on Complex I Biogenesis: Implications for Metabolic Disease." In Mitochondrial DNA, Mitochondria, Disease and Stem Cells, 25–47. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-101-1_2.

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Stavridis, Marios P. "Embryonic Stem Cells: A Signalling Perspective." In Mitochondrial DNA, Mitochondria, Disease and Stem Cells, 49–68. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-101-1_3.

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Ramalho-Santos, João, and Ana Sofia Rodrigues. "From Oocytes and Pluripotent Stem Cells to Fully Differentiated Fates: (Also) a Mitochondrial Odyssey." In Mitochondrial DNA, Mitochondria, Disease and Stem Cells, 69–86. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-101-1_4.

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Facucho-Oliveira, João, Tejal Kulkarni, Gisela Machado-Oliveira, and Justin C. St. John. "From Pluripotency to Differentiation: The Role of mtDNA in Stem Cell Models of Mitochondrial Diseases." In Mitochondrial DNA, Mitochondria, Disease and Stem Cells, 87–118. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-101-1_5.

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Kelly, Richard D. W., Arsalan Mahmud, and Justin C. St. John. "Assisted Reproductive Technologies: The Potential to Prevent the Transmission of Mutant mtDNA from One Generation to the Next." In Mitochondrial DNA, Mitochondria, Disease and Stem Cells, 157–83. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-101-1_7.

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Asahi, Tadashi, Masayodhi Maeshima, Tsuyoshi Nakagawa, Kazuto Kobayashi, Yukimoto Iwasaki, and Kenzo Nakamura. "Synthesis of the Nuclear DNA-Encoded Subunits of Higher Plant Cytochrome C Oxidase and F1ATPase." In Plant Mitochondria, 265–74. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-3517-5_45.

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Pan, Yue, Min Cao, Jianzhou Liu, Qing Yang, Xiaoyu Miao, Vay Liang W. Go, Paul W. N. Lee, and Gary Guishan Xiao. "Metabolic Regulation in Mitochondria and Drug Resistance." In Mitochondrial DNA and Diseases, 149–71. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-6674-0_11.

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Conference papers on the topic "Mitochondria. DNA"

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Konstantinov, Yu M., M. V. Koulintchenko, E. S. Klimenko, N. A. Bolotova, V. I. Tarasenko, and V. N. Shmakov. "STUDYING OF DNA IMPORT FACTORS IN PLANT MITOCHONDRIA." In The Second All-Russian Scientific Conference with international participation "Regulation Mechanisms of Eukariotic Cell Organelle Functions". SIPPB SB RAS, 2018. http://dx.doi.org/10.31255/978-5-94797-318-1-55-57.

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Klimenko, E. S., V. N. Shmakov, N. A. Bolotova, I. Yu Subota, V. I. Tarasenko, M. V. Koulintchenko, and Yu M. Konstantinov. "STUDY OF DNA IMPORT INTO PLANT MITOCHONDRIA USING THE RECONSTRUCTION METHOD." In The All-Russian Scientific Conference with International Participation and Schools of Young Scientists "Mechanisms of resistance of plants and microorganisms to unfavorable environmental". SIPPB SB RAS, 2018. http://dx.doi.org/10.31255/978-5-94797-319-8-1272-1275.

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Konstantinov, Y. M., Т. А. Bolotova, A. Dietrich, F. Weber-Lotfi, and M. V. Koulintchenko. "STUDYING OF DIFFERENT LENGTH AND STRUCTURE DNA IMPORT INTO PLANT MITOCHONDRIA." In The All-Russian Scientific Conference with International Participation and Schools of Young Scientists "Mechanisms of resistance of plants and microorganisms to unfavorable environmental". SIPPB SB RAS, 2018. http://dx.doi.org/10.31255/978-5-94797-319-8-1276-1279.

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Tarasenko, V. I., T. A. Bolotova, M. V. Koulintchenko, and Y. M. Konstantinov. "STUDY OF DNA IMPORT INTO MITOCHONDRIA IN VIVO USING ARABIDOPSIS PROTOPLASTS." In The All-Russian Scientific Conference with International Participation and Schools of Young Scientists "Mechanisms of resistance of plants and microorganisms to unfavorable environmental". SIPPB SB RAS, 2018. http://dx.doi.org/10.31255/978-5-94797-319-8-1385-1387.

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Kresovich, Jacob K., Tao Gao, Brian T. Joyce, Pantel Vokonas, Joel Schwartz, Andrea A. Baccarelli, and Lifang Hou. "Abstract 4251: DNA methylation of mitochondrial biogenesis regulating genes: A possible link between telomeres, mitochondria, and cancer incidence." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4251.

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Tarasenko, V. I., M. V. Kulinchenko, E. S. Klimenko, T. I. Tarasenko, I. Yu Subota, V. N. Shmakov, and Yu M. Konstantinov. "Import of DNA into plant mitochondria: relationship with genetic and physiological processes." In IX Congress of society physiologists of plants of Russia "Plant physiology is the basis for creating plants of the future". Kazan University Press, 2019. http://dx.doi.org/10.26907/978-5-00130-204-9-2019-424.

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Liu, G., S. Soberanes, N. Bruce, SA Weitzman, GR Budinger, PT Schumacker, and DW Kamp. "A Mitochondria-Targeted DNA Repair Enzyme, hOgg1, Prevents Oxidant-Induced Alveolar Epithelial Cell Apoptosis by Chaperoning and Preserving Mitochondrial Aconitase." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4178.

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Kamaluddin, Siti Norsyuhada, Salmah Yaakop, Wan Mohd Razi Idris, Jeffrine Japning Rovie-Ryan, and Badrul Munir Md-Zain. "Subspecies identification of captive Orang Utan in Melaka based on D-loop mitochondria DNA." In THE 2017 UKM FST POSTGRADUATE COLLOQUIUM: Proceedings of the University Kebangsaan Malaysia, Faculty of Science and Technology 2017 Postgraduate Colloquium. Author(s), 2018. http://dx.doi.org/10.1063/1.5027970.

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Klimenko, E. S., V. N. Shmakov, T. A. Bolotova, I. Yu Subota, V. I. Tarasenko, M. V. Koulintchenko, and Yu M. Konstantinov. "STUDYING OF ROLE OF THE INTERACTION BETWEEN MITOCHONDRIA MEMBRANES AND ENDOPLASMATIC RETICULUM IN DNA IMPORT." In The Second All-Russian Scientific Conference with international participation "Regulation Mechanisms of Eukariotic Cell Organelle Functions". SIPPB SB RAS, 2018. http://dx.doi.org/10.31255/978-5-94797-318-1-49-51.

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"DNA import into plant mitochondria: studying of the translocation pathways in organello and in vivo." In Plant Genetics, Genomics, Bioinformatics, and Biotechnology. Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 2019. http://dx.doi.org/10.18699/plantgen2019-189.

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Reports on the topic "Mitochondria. DNA"

1

Friddle, R. W., J. E. Klare, A. Noy, M. Corzett, R. Balhorn, R. J. Baskin, S. S. Martin, and E. P. Baldwin. DNA Compaction by Yeast Mitochondrial Protein ABF2p. Office of Scientific and Technical Information (OSTI), May 2003. http://dx.doi.org/10.2172/15007313.

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Mathews, Christopher K. DNA Precursor Metabolism and Mitochondrial Genome Stability. Fort Belvoir, VA: Defense Technical Information Center, April 2003. http://dx.doi.org/10.21236/ada460347.

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SAlly A. Mackenzie. Proteomic Dissection of the Mitochondrial DNA Metabolism Apparatus in Arabidopsis. Office of Scientific and Technical Information (OSTI), January 2004. http://dx.doi.org/10.2172/835670.

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Hsieh, Jer-Tsong. Suppression of BRCA2 by Mutant Mitochondrial DNA in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, February 2012. http://dx.doi.org/10.21236/ada564267.

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Hsieh, Jer-Tsong. Suppression of BRCA2 by Mutant Mitochondrial DNA in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2013. http://dx.doi.org/10.21236/ada585765.

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Hsieh, Jer-Tsong. Suppression of BRCA2 by Mutant Mitochondrial DNA in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2011. http://dx.doi.org/10.21236/ada549344.

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Stevens, Tracy. Analysis of mitochondrial DNA restriction fragment patterns in killer whales, Orcinus orca. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.5812.

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Haddad, Bassem R. Detection of Mitochondrial DNA Mutations in Mammary Epithelial Cells in Nipple Aspirate Fluid. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada434094.

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Haddad, Bassem R. Detection of Mitochondrial DNA Mutations in Mammary Epithelial Cells in Nipple Aspirate Fluid. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412041.

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Haddad, Bassem R. Detection of Mitochondrial DNA Mutations in Mammary Epithelial Cells in Nipple Aspirate Fluid. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada423469.

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