Bibliografías temáticas / Mitochondrial DNA

Literatura académica sobre el tema "Mitochondrial DNA"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 31 de julio de 2024

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Artículos de revistas sobre el tema "Mitochondrial DNA"

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Faria, Rúben, Eric Vivés, Prisca Boisguerin, Angela Sousa y Diana Costa. "Development of Peptide-Based Nanoparticles for Mitochondrial Plasmid DNA Delivery". Polymers 13, n.º 11 (1 de junio de 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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Basu, Urmimala, Alicia M. Bostwick, Kalyan Das, Kristin E. Dittenhafer-Reed y Smita S. Patel. "Structure, mechanism, and regulation of mitochondrial DNA transcription initiation". Journal of Biological Chemistry 295, n.º 52 (30 de octubre de 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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3

Campbell, C. L. y P. E. Thorsness. "Escape of mitochondrial DNA to the nucleus in yme1 yeast is mediated by vacuolar-dependent turnover of abnormal mitochondrial compartments". Journal of Cell Science 111, n.º 16 (15 de agosto de 1998): 2455–64. http://dx.doi.org/10.1242/jcs.111.16.2455.

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Inactivation of Yme1p, a mitochondrially-localized ATP-dependent metallo-protease in the yeast Saccharomyces cerevisiae, causes a high rate of DNA escape from mitochondria to the nucleus as well as pleiotropic functional and morphological mitochondrial defects. The evidence presented here suggests that the abnormal mitochondria of a yme1 strain are degraded by the vacuole. First, electron microscopy of Yme1p-deficient strains revealed mitochondria physically associated with the vacuole via electron dense structures. Second, disruption of vacuolar function affected the frequency of mitochondrial DNA escape from yme1 and wild-type strains. Both PEP4 or PRC1 gene disruptions resulted in a lower frequency of mitochondrial DNA escape. Third, an in vivo assay that monitors vacuole-dependent turnover of the mitochondrial compartment demonstrated an increased rate of mitochondrial turnover in yme1 yeast when compared to the rate found in wild-type yeast. In this assay, vacuolar alkaline phosphatase, encoded by PHO8, was targeted to mitochondria in a strain bearing disruption to the genomic PHO8 locus. Maturation of the mitochondrially localized alkaline phosphatase pro-enzyme requires proteinase A, which is localized in the vacuole. Therefore, alkaline phosphatase activity reflects vacuole-dependent turnover of mitochondria. This assay reveals that mitochondria of a yme1 strain are taken up by the vacuole more frequently than mitochondria of an isogenic wild-type strain when these yeast are cultured in medium necessitating respiratory growth. Degradation of abnormal mitochondria is one pathway by which mitochondrial DNA escapes and migrates to the nucleus.
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Herrmann, J. M., R. A. Stuart, E. A. Craig y W. Neupert. "Mitochondrial heat shock protein 70, a molecular chaperone for proteins encoded by mitochondrial DNA." Journal of Cell Biology 127, n.º 4 (15 de noviembre de 1994): 893–902. http://dx.doi.org/10.1083/jcb.127.4.893.

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Mitochondrial heat shock protein 70 (mt-Hsp70) has been shown to play an important role in facilitating import into, as well as folding and assembly of nuclear-encoded proteins in the mitochondrial matrix. Here, we describe a role for mt-Hsp70 in chaperoning proteins encoded by mitochondrial DNA and synthesized within mitochondria. The availability of mt-Hsp70 function influences the pattern of proteins synthesized in mitochondria of yeast both in vivo and in vitro. In particular, we show that mt-Hsp70 acts in maintaining the var1 protein, the only mitochondrially encoded subunit of mitochondrial ribosomes, in an assembly competent state, especially under heat stress conditions. Furthermore, mt-Hsp70 helps to facilitate assembly of mitochondrially encoded subunits of the ATP synthase complex. By interacting with the ATP-ase 9 oligomer, mt-Hsp70 promotes assembly of ATP-ase 6, and thereby protects the latter protein from proteolytic degradation. Thus mt-Hsp70 by acting as a chaperone for proteins encoded by the mitochondrial DNA, has a critical role in the assembly of supra-molecular complexes.
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5

Varma, V. A., C. M. Cerjan, K. L. Abbott y S. B. Hunter. "Non-isotopic in situ hybridization method for mitochondria in oncocytes." Journal of Histochemistry & Cytochemistry 42, n.º 2 (febrero de 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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6

Habbane, Mouna, Julio Montoya, Taha Rhouda, Yousra Sbaoui, Driss Radallah y Sonia Emperador. "Human Mitochondrial DNA: Particularities and Diseases". Biomedicines 9, n.º 10 (1 de octubre de 2021): 1364. http://dx.doi.org/10.3390/biomedicines9101364.

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Mitochondria are the cell’s power site, transforming energy into a form that the cell can employ for necessary metabolic reactions. These organelles present their own DNA. Although it codes for a small number of genes, mutations in mtDNA are common. Molecular genetics diagnosis allows the analysis of DNA in several areas such as infectiology, oncology, human genetics and personalized medicine. Knowing that the mitochondrial DNA is subject to several mutations which have a direct impact on the metabolism of the mitochondrion leading to many diseases, it is therefore necessary to detect these mutations in the patients involved. To date numerous mitochondrial mutations have been described in humans, permitting confirmation of clinical diagnosis, in addition to a better management of the patients. Therefore, different techniques are employed to study the presence or absence of mitochondrial mutations. However, new mutations are discovered, and to determine if they are the cause of disease, different functional mitochondrial studies are undertaken using transmitochondrial cybrid cells that are constructed by fusion of platelets of the patient that presents the mutation, with rho osteosarcoma cell line. Moreover, the contribution of next generation sequencing allows sequencing of the entire human genome within a single day and should be considered in the diagnosis of mitochondrial mutations.
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7

Hong, Seongho, Sanghun Kim, Kyoungmi Kim y Hyunji Lee. "Clinical Approaches for Mitochondrial Diseases". Cells 12, n.º 20 (20 de octubre de 2023): 2494. http://dx.doi.org/10.3390/cells12202494.

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Mitochondria are subcontractors dedicated to energy production within cells. In human mitochondria, almost all mitochondrial proteins originate from the nucleus, except for 13 subunit proteins that make up the crucial system required to perform ‘oxidative phosphorylation (OX PHOS)’, which are expressed by the mitochondria’s self-contained DNA. Mitochondrial DNA (mtDNA) also encodes 2 rRNA and 22 tRNA species. Mitochondrial DNA replicates almost autonomously, independent of the nucleus, and its heredity follows a non-Mendelian pattern, exclusively passing from mother to children. Numerous studies have identified mtDNA mutation-related genetic diseases. The consequences of various types of mtDNA mutations, including insertions, deletions, and single base-pair mutations, are studied to reveal their relationship to mitochondrial diseases. Most mitochondrial diseases exhibit fatal symptoms, leading to ongoing therapeutic research with diverse approaches such as stimulating the defective OXPHOS system, mitochondrial replacement, and allotropic expression of defective enzymes. This review provides detailed information on two topics: (1) mitochondrial diseases caused by mtDNA mutations, and (2) the mechanisms of current treatments for mitochondrial diseases and clinical trials.
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Wang, Sheng-Fan, Shiuan Chen, Ling-Ming Tseng y Hsin-Chen Lee. "Role of the mitochondrial stress response in human cancer progression". Experimental Biology and Medicine 245, n.º 10 (23 de abril de 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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Bradshaw, Patrick C. y David C. Samuels. "A computational model of mitochondrial deoxynucleotide metabolism and DNA replication". American Journal of Physiology-Cell Physiology 288, n.º 5 (mayo de 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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10

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 (31 de diciembre de 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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Tesis sobre el 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.

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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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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.

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Les maladies mitochondriales regroupent un ensemble de pathologies liées à un déficit de la chaînerespiratoire mitochondriale. Au laboratoire, nous focalisons notre intérêt sur les mitochondriopathies liées à undéfaut de stabilité de l’ADN mitochondrial (ADNmt), qui se traduit par des délétions multiples et/ou unedéplétion (diminution du nombre de copies). Ces pathologies sont caractérisées par une importantehétérogénéité clinique et génétique et sont secondaires à des mutations dans des gènes nucléaires codantpour des protéines impliquées dans le maintien de l’ADNmt. De nos jours, la recherche des gènesresponsables d’instabilité de l’ADNmt s’avère négative chez plus de 70% des malades, d’où un grand intérêtpour améliorer les techniques d’identification des mutations et la recherche de nouveaux gènes impliquésdans ces pathologies
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3

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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4

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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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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Berg, 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.

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Les maladies mitochondriales regroupent un ensemble de pathologies liées à un déficit de la chaînerespiratoire mitochondriale. Au laboratoire, nous focalisons notre intérêt sur les mitochondriopathies liées à undéfaut de stabilité de l’ADN mitochondrial (ADNmt), qui se traduit par des délétions multiples et/ou unedéplétion (diminution du nombre de copies). Ces pathologies sont caractérisées par une importantehétérogénéité clinique et génétique et sont secondaires à des mutations dans des gènes nucléaires codantpour des protéines impliquées dans le maintien de l’ADNmt. De nos jours, la recherche des gènesresponsables d’instabilité de l’ADNmt s’avère négative chez plus de 70% des malades, d’où un grand intérêtpour améliorer les techniques d’identification des mutations et la recherche de nouveaux gènes impliquésdans ces pathologies
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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.

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Myers, K. A. "Alkylation of mitochondrial DNA". Thesis, University of Manchester, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234216.

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Johansson, 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.

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This mini-review investigates and compiles the latest knowledge regarding epigenetic changes on the mammalian mitochondrial DNA and its proteins. Methylation of the DNA, acetylation of the proteins and silencing of genes by short non-coding RNAs are the main epigenetic changes known today to affect mitochondrial DNA, mostly leading to repression. Methylation mainly occurs at non-CpG sites in the main non-coding region called the D-loop, with methylation patterns being cell type specific. Acetylation of proteins are mainly controlled by the deacetylase SIRT3, with its function being correlated to longevity. On the other hand, mitochondrial dysfunction is directly associated with a plethora of diseases, such as neurodegenerative disorders and heart disorders. The mitochondrion and nucleus are immensely dependent on each other and exchange vital proteins and RNAs, with epigenetic changes on one potentially affecting the other. Recent research shows that heteroplasmy is a proven cause of mitochondrial malfunction and that paternal inheritance is possible. The mitochondrial haplotype also shows different vulnerability to certain diets and diseases, leading to the conclusion that the mitochondrial haplotype can be used to more than just tracing human origins, such as to predicting and preventing diseases.
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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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Libros sobre el tema "Mitochondrial DNA"

1

Copeland, William C. Mitochondrial DNA. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592592848.

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Stuart, Jeffrey A., ed. Mitochondrial DNA. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-521-3.

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McKenzie, Matthew, ed. Mitochondrial DNA. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3040-1.

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Nicholls, Thomas J., Jay P. Uhler y Maria Falkenberg, eds. Mitochondrial DNA. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2922-2.

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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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S, DiMauro y Wallace Douglas C, eds. Mitochondrial DNA in human pathology. New York: Raven Press, 1993.

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James, Holt Ian, ed. Genetics of mitochondrial diseases. Oxford: Oxford University Press, 2003.

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Sun, Hongzhi y Xiangdong Wang, eds. Mitochondrial DNA and Diseases. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-6674-0.

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A, Dudareva N. y Salganik, R. I. (Rudolʹf Iosifovich), eds. Mitokhondrialʹnyĭ genom. Novosibirsk: "Nauka," Sibirskoe otd-nie, 1990.

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Capítulos de libros sobre el tema "Mitochondrial DNA"

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Mainieri, Avantika. "Mitochondrial DNA". En Encyclopedia of Evolutionary Psychological Science, 1–4. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-16999-6_2229-1.

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Verma, Mukesh y Deepak Kumar. "Mitochondrial DNA". En Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_3765-2.

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Verma, Mukesh y Deepak Kumar. "Mitochondrial DNA". En Encyclopedia of Cancer, 2867–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_3765.

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Mishra, Alaknanda. "Mitochondrial DNA". En Encyclopedia of Animal Cognition and Behavior, 4329–32. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-319-55065-7_162.

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Verma, Mukesh y Deepak Kumar. "Mitochondrial DNA". En Encyclopedia of Cancer, 2331–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3765.

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Mishra, Alaknanda. "Mitochondrial DNA". En Encyclopedia of Animal Cognition and Behavior, 1–4. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47829-6_162-1.

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Mainieri, Avantika. "Mitochondrial DNA". En Encyclopedia of Evolutionary Psychological Science, 5150–52. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-19650-3_2229.

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Gojobori, Jun. "Mitochondrial DNA". En Evolution of the Human Genome II, 103–20. Tokyo: Springer Japan, 2021. http://dx.doi.org/10.1007/978-4-431-56904-6_4.

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Reynier, P., Y. Malthièry y P. Lestienne. "Mitochondrial DNA Analysis". En Mitochondrial Diseases, 379–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59884-5_28.

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Casane, D. y M. Guéride. "Mitochondrial DNA Inheritance in Mammals". En Mitochondrial Diseases, 17–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59884-5_3.

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Actas de conferencias sobre el tema "Mitochondrial DNA"

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Joseph Mathuram, T. L., Y. Su, M. Hatzoglou, Y. Perry, Y. Wu y A. Blumental-Perry. "Mitochondria-to-Nucleus Retrograde Signaling Via Mitochondrial DNA Encoded Non-coding RNA Regulates Mitochondrial Bioenergetics". En American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a4400.

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Cristea, Paul Dan y Rodica Tuduce. "Mitochondrial DNA Analysis Using Genomic Signals". En 2009 16th International Conference on Systems, Signals and Image Processing. IEEE, 2009. http://dx.doi.org/10.1109/iwssip.2009.5367711.

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Nesbitt, V. y R. McFarland. "G259 Mitochondrial DNA disease in children". En Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference and exhibition, 13–15 May 2019, ICC, Birmingham, Paediatrics: pathways to a brighter future. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-rcpch.251.

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Xu, W., R. Chen, B. Hu, J. G. Zein, C. Liu, S. A. A. Comhair, M. A. Aldred et al. "Mitochondrial DNA Variation and Severe Asthma". En American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2961.

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Melamud, M. M., E. A. Ermakov, P. I. Brit, E. S. Zhuravlev, E. A. Balakhonova, G. A. Stepanov, D. A. Kamaeva, S. A. Ivanova, G. A. Nevinsky y V. N. Buneva. "ASSOCIATION BETWEEN HIGH CONCENTRATIONS OF CIRCULATING CELL-FREE DNA AND SUICIDE ATTEMPTS IN SCHIZOPHRENIA". En X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-347.

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The paper presents the results of measuring the concentration of total, nuclear and mitochondrial circulating cell-free DNA in blood plasma in schizophrenia. It has been shown that the concentration of total and nuclear, but not mitochondrial cell-free DNA, is significantly higher in patients with a history of suicide attempts compared to patients without suicide attempts and healthy individuals without mental pathology
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Wan, Emily S., Michael H. Cho, Nadia Boutaoui, Barbara J. Klanderman, Jody S. Sylvia, John P. Ziniti, Augusto A. Litonjua et al. "Mitochondrial DNA Polymorphisms Are Associated With COPD". En American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2921.

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Aggarwal, S., I. Ahmad, S. Gu, H. Paiste, M. N. Gillespie y S. Matalon. "Mitochondrial DNA Repair Ameliorates Inhalation Lung Injury". En American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1020.

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van den Heuvel, Robert. "Mitochondrial DNA levels predict COVID-19 severity". En ATS 2023 International Conference, editado por Rachel Giles. Baarn, the Netherlands: Medicom Medical Publishers, 2023. http://dx.doi.org/10.55788/e3a1fb1a.

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Cristea, Paul Dan y Rodica Tuduce. "Nucleotide Genomic Signal analysis of hominidae mitochondrial DNA". En 2009 16th International Conference on Digital Signal Processing (DSP). IEEE, 2009. http://dx.doi.org/10.1109/icdsp.2009.5201251.

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Kulvinder Singh Mann y Navjot Kaur. "Mitochondrial DNA for Bio-molecular Archaeology of mummies". En 2015 IEEE International Conference on Electrical, Computer and Communication Technologies (ICECCT). IEEE, 2015. http://dx.doi.org/10.1109/icecct.2015.7226105.

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Informes sobre el tema "Mitochondrial DNA"

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Friddle, R. W., J. E. Klare, A. Noy, M. Corzett, R. Balhorn, R. J. Baskin, S. S. Martin y E. P. Baldwin. DNA Compaction by Yeast Mitochondrial Protein ABF2p. Office of Scientific and Technical Information (OSTI), mayo de 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, abril de 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), enero de 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, febrero de 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, mayo de 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, mayo de 2011. http://dx.doi.org/10.21236/ada549344.

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Izhar, Shamay y Maureen Hanson. Expression of Mitochondrial DNA Associated with Cytoplasmic Male Sterility in Petunia. United States Department of Agriculture, julio de 1987. http://dx.doi.org/10.32747/1987.7566866.bard.

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Izhar, Shamay, Maureen Hanson y Nurit Firon. Expression of the Mitochondrial Locus Associated with Cytoplasmic Male Sterility in Petunia. United States Department of Agriculture, febrero de 1996. http://dx.doi.org/10.32747/1996.7604933.bard.

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The main goal of the proposed research was to continue the mutual investigations into the molecular basis of CMS and male fertility restoration [MRF], with the ultimate goal of understanding these phenomena in higher plants. The experiments focused on: (1) dissecting apart the complex CMS - specific mitochondrial S-Pcf locus, in order to distinguish its essential parts which cause sterility from other parts and study its molecular evolution. (2) Studying the expression of the various regions of the S-Pcf locus in fertile and sterile lines and comparing the structure and ultrastructure of sterile and fertile tissues. (3) Determine whether alteration in respiration is genetically associated with CMS. Our mutual investigations further substantiated the association between the S-Pcf locus and CMS by the findings that the fertile phenotype of a population of unstable petunia somatic hybrids which contain the S-Pcf locus, is due to the presence of multiple muclear fertility restoration genes in this group of progenies. The information obtained by our studies indicate that homologous recombination played a major role in the molecular evolution of the S-Pcf locus and the CMS trait and in the generation of mitochondrial mutations in general. Our data suggest that the CMS cytoplasm evolved by introduction of a urs-s containing sublimon into the main mitochondrial genome via homologous recombination. We have also found that the first mutation detected so far in S-Pcf is a consequence of a homologous recombination mechanism involving part of the cox2 coding sequence. In all the cases studied by us, at the molecular level, we found that fusion of two different cells caused mitochondrial DNA recombination followed by sorting out of a specific mtDNA population or sequences. This sequence of events suggested as a mechanism for the generation of novel mitochondrial genomes and the creation of new traits. The present research also provides data concerning the expression of the recombined and complex CMS-specific S-Pcf locus as compared with the expression of additional mitochondrial proteins as well as comparative histological and ultrastructural studies of CMS and fertile Petunia. Evidence is provided for differential localization of mitochondrially encoded proteins in situ at the tissue level. The similar localization patterns of Pcf and atpA may indicate that Pcf product could interfere with the functioning of the mitochondrial ATPase in a tissue undergoing meiosis and microsporogenesis. Studies of respiration in CMS and fertile Petunia lines indicate that they differe in the partitioning of electron transport through the cytochrome oxidase and alternative oxidase pathways. The data indicate that the electron flux through the two oxidase pathways differs between mitochondria from fertile and sterile Petunia lines at certain redox states of the ubiquinone pool. In summary, extensive data concerning the CMS-specific S-Pcf locus of Petunia at the DNA and protein levels as well as information concerning different biochemical activity in CMS as compared to male fertile lines have been accumulated during the three years of this project. In addition, the involvement of the homologous recombination mechanism in the evolution of mt encoded traits is emphasized.
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Stevens, Tracy. Analysis of mitochondrial DNA restriction fragment patterns in killer whales, Orcinus orca. Portland State University Library, enero de 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, septiembre de 2004. http://dx.doi.org/10.21236/ada434094.

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