Academic literature on the topic 'Transmission mitochondriale'
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Journal articles on the topic "Transmission mitochondriale"
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Wilhelm, J. M., B. Mousson de Camaret, A. Derragui, R. Dukic, P. Thannberger, O. Saraceni, and P. Kieffer. "Ophtalmoplégie progressive chronique ≪ plus ≫d'origine mitochondriale à transmission autosomique dominante." La Revue de Médecine Interne 24 (December 2003): 465s. http://dx.doi.org/10.1016/s0248-8663(03)80555-6.
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Angers, Annie, Philip Ouimet, Assia Tsyvian-Dzyabko, Tanya Nock, and Sophie Breton. "L’ADN mitochondrial, un potentiel codant mésestimé." médecine/sciences 35, no. 1 (January 2019): 46–54. http://dx.doi.org/10.1051/medsci/2018308.
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Du génome bactérien de l’endosymbionte d’origine les mitochondries animales n’ont retenu que 13 séquences codant des polypeptides essentiels à la production d’ATP. La découverte de petits peptides d’origine mitochondriale vient remettre en question cette interprétation du génome des mitochondries et suggère que leur potentiel codant reste sous-estimé. L’humanine, MOTS-c, les SHLP et Gau sont des peptides dérivés de l’ADN mitochondrial dont l’existence a été démontrée expérimentalement et qui jouent des rôles importants dans la régulation de l’apoptose et du métabolisme cellulaire. Chez certains bivalves à transmission doublement uniparentale des mitochondries, des gènes codant des peptides additionnels ont été découverts et pourraient être impliqués dans la détermination du sexe de ces animaux.
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Pierry, C., T. Trian, E. Maurat, R. Marthan, P. O. Girodet, and P. Berger. "Ultrastructure mitochondriale du muscle lisse bronchique chez l’asthmatique sévère et non sévère : étude quantitative en microscopie électronique à transmission." Revue des Maladies Respiratoires 34 (January 2017): A328—A329. http://dx.doi.org/10.1016/j.rmr.2016.10.868.
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Pierry, C., T. Trian, E. Maurat, R. Marthan, P. O. Girodet, and P. Berger. "Ultrastructure mitochondriale du muscle lisse bronchique chez l’asthmatique sévère et non sévère : étude quantitative en miscroscopie électronique à transmission." Revue des Maladies Respiratoires 34 (January 2017): A26—A27. http://dx.doi.org/10.1016/j.rmr.2016.10.056.
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Wilhelm, J. M., B. Mousson de Camret, S. Rozan-Rodier, A. Derragui, P. Thannberger, and O. Saraceni. "P120 Diabète associé à une cytopathie mitochondriale à transmission autosomique dominante. À propos d’un cas de mutation du gène nucléaire Twinkle." Diabetes & Metabolism 35 (March 2009): A56. http://dx.doi.org/10.1016/s1262-3636(09)71918-4.
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Yancey, Danielle M., Jason L. Guichard, Mustafa I. Ahmed, Lufang Zhou, Michael P. Murphy, Michelle S. Johnson, Gloria A. Benavides, James Collawn, Victor Darley-Usmar, and Louis J. Dell'Italia. "Cardiomyocyte mitochondrial oxidative stress and cytoskeletal breakdown in the heart with a primary volume overload." American Journal of Physiology-Heart and Circulatory Physiology 308, no. 6 (March 15, 2015): H651—H663. http://dx.doi.org/10.1152/ajpheart.00638.2014.
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Left ventricular (LV) volume overload (VO) results in cardiomyocyte oxidative stress and mitochondrial dysfunction. Because mitochondria are both a source and target of ROS, we hypothesized that the mitochondrially targeted antioxidant mitoubiquinone (MitoQ) will improve cardiomyocyte damage and LV dysfunction in VO. Isolated cardiomyocytes from Sprague-Dawley rats were exposed to stretch in vitro and VO of aortocaval fistula (ACF) in vivo. ACF rats were treated with and without MitoQ. Isolated cardiomyocytes were analyzed after 3 h of cyclical stretch or 8 wk of ACF with MitoSox red or 5-(and-6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate to measure ROS and with tetramethylrhodamine to measure mitochondrial membrane potential. Transmission electron microscopy and immunohistochemistry were used for cardiomyocyte structural assessment. In vitro cyclical stretch and 8-wk ACF resulted in increased cardiomyocyte mitochondrial ROS production and decreased mitochondrial membrane potential, which were significantly improved by MitoQ. ACF had extensive loss of desmin and β2-tubulin that was paralleled by mitochondrial disorganization, loss of cristae, swelling, and clustering identified by mitochondria complex IV staining and transmission electron microscopy. MitoQ improved mitochondrial structural damage and attenuated desmin loss/degradation evidenced by immunohistochemistry and protein expression. However, LV dilatation and fractional shortening were unaffected by MitoQ treatment in 8-wk ACF. In conclusion, although MitoQ did not affect LV dilatation or function in ACF, these experiments suggest a connection of cardiomyocyte mitochondria-derived ROS production with cytoskeletal disruption and mitochondrial damage in the VO of ACF.
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Medler, Kathryn, and Evanna L. Gleason. "Mitochondrial Ca2+ Buffering Regulates Synaptic Transmission Between Retinal Amacrine Cells." Journal of Neurophysiology 87, no. 3 (March 1, 2002): 1426–39. http://dx.doi.org/10.1152/jn.00627.2001.
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The diverse functions of retinal amacrine cells are reliant on the physiological properties of their synapses. Here we examine the role of mitochondria as Ca2+ buffering organelles in synaptic transmission between GABAergic amacrine cells. We used the protonophore p-trifluoromethoxy-phenylhydrazone (FCCP) to dissipate the membrane potential across the inner mitochondrial membrane that normally sustains the activity of the mitochondrial Ca2+ uniporter. Measurements of cytosolic Ca2+ levels reveal that prolonged depolarization-induced Ca2+ elevations measured at the cell body are altered by inhibition of mitochondrial Ca2+ uptake. Furthermore, an analysis of the ratio of Ca2+ efflux on the plasma membrane Na-Ca exchanger to influx through Ca2+ channels during voltage steps indicates that mitochondria can also buffer Ca2+ loads induced by relatively brief stimuli. Importantly, we also demonstrate that mitochondrial Ca2+ uptake operates at rest to help maintain low cytosolic Ca2+ levels. This aspect of mitochondrial Ca2+ buffering suggests that in amacrine cells, the normal function of Ca2+-dependent mechanisms would be contingent upon ongoing mitochondrial Ca2+ uptake. To test the role of mitochondrial Ca2+ buffering at amacrine cell synapses, we record from amacrine cells receiving GABAergic synaptic input. The Ca2+ elevations produced by inhibition of mitochondrial Ca2+uptake are localized and sufficient in magnitude to stimulate exocytosis, indicating that mitochondria help to maintain low levels of exocytosis at rest. However, we found that inhibition of mitochondrial Ca2+ uptake during evoked synaptic transmission results in a reduction in the charge transferred at the synapse. Recordings from isolated amacrine cells reveal that this is most likely due to the increase in the inactivation of presynaptic Ca2+ channels observed in the absence of mitochondrial Ca2+ buffering. These results demonstrate that mitochondrial Ca2+ buffering plays a critical role in the function of amacrine cell synapses.
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Kitazaki, Kazuyoshi, and Tomohiko Kubo. "Cost of Having the Largest Mitochondrial Genome: Evolutionary Mechanism of Plant Mitochondrial Genome." Journal of Botany 2010 (May 30, 2010): 1–12. http://dx.doi.org/10.1155/2010/620137.
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The angiosperm mitochondrial genome is the largest and least gene-dense among the eukaryotes, because its intergenic regions are expanded. There seems to be no functional constraint on the size of the intergenic regions; angiosperms maintain the large mitochondrial genome size by a currently unknown mechanism. After a brief description of the angiosperm mitochondrial genome, this review focuses on our current knowledge of the mechanisms that control the maintenance and alteration of the genome. In both processes, the control of homologous recombination is crucial in terms of site and frequency. The copy numbers of various types of mitochondrial DNA molecules may also be controlled, especially during transmission of the mitochondrial genome from one generation to the next. An important characteristic of angiosperm mitochondria is that they contain polypeptides that are translated from open reading frames created as byproducts of genome alteration and that are generally nonfunctional. Such polypeptides have potential to evolve into functional ones responsible for mitochondrially encoded traits such as cytoplasmic male sterility or may be remnants of the former functional polypeptides.
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Aretz, Ina, Christopher Jakubke, and Christof Osman. "Power to the daughters – mitochondrial and mtDNA transmission during cell division." Biological Chemistry 401, no. 5 (April 28, 2020): 533–46. http://dx.doi.org/10.1515/hsz-2019-0337.
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AbstractMitochondria supply virtually all eukaryotic cells with energy through ATP production by oxidative phosphoryplation (OXPHOS). Accordingly, maintenance of mitochondrial function is fundamentally important to sustain cellular health and various diseases have been linked to mitochondrial dysfunction. Biogenesis of OXPHOS complexes crucially depends on mitochondrial DNA (mtDNA) that encodes essential subunits of the respiratory chain and is distributed in multiple copies throughout the mitochondrial network. During cell division, mitochondria, including mtDNA, need to be accurately apportioned to daughter cells. This process requires an intimate and coordinated interplay between the cell cycle, mitochondrial dynamics and the replication and distribution of mtDNA. Recent years have seen exciting advances in the elucidation of the mechanisms that facilitate these processes and essential key players have been identified. Moreover, segregation of qualitatively distinct mitochondria during asymmetric cell division is emerging as an important quality control step, which secures the maintenance of a healthy cell population.
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Su, Bo, Yun-Song Ji, Xu-lu Sun, Xiang-Hua Liu, and Zhe-Yu Chen. "Brain-derived Neurotrophic Factor (BDNF)-induced Mitochondrial Motility Arrest and Presynaptic Docking Contribute to BDNF-enhanced Synaptic Transmission." Journal of Biological Chemistry 289, no. 3 (December 3, 2013): 1213–26. http://dx.doi.org/10.1074/jbc.m113.526129.
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Appropriate mitochondrial transport and distribution are essential for neurons because of the high energy and Ca2+ buffering requirements at synapses. Brain-derived neurotrophic factor (BDNF) plays an essential role in regulating synaptic transmission and plasticity. However, whether and how BDNF can regulate mitochondrial transport and distribution are still unclear. Here, we find that in cultured hippocampal neurons, application of BDNF for 15 min decreased the percentage of moving mitochondria in axons, a process dependent on the activation of the TrkB receptor and its downstream PI3K and phospholipase-Cγ signaling pathways. Moreover, the BDNF-induced mitochondrial stopping requires the activation of transient receptor potential canonical 3 and 6 (TRPC3 and TRPC6) channels and elevated intracellular Ca2+ levels. The Ca2+ sensor Miro1 plays an important role in this process. Finally, the BDNF-induced mitochondrial stopping leads to the accumulation of more mitochondria at presynaptic sites. Mutant Miro1 lacking the ability to bind Ca2+ prevents BDNF-induced mitochondrial presynaptic accumulation and synaptic transmission, suggesting that Miro1-mediated mitochondrial motility is involved in BDNF-induced mitochondrial presynaptic docking and neurotransmission. Together, these data suggest that mitochondrial transport and distribution play essential roles in BDNF-mediated synaptic transmission.
Dissertations / Theses on the topic "Transmission mitochondriale"
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Sternberg, Damien. "Contribution à trois aspects de la génétique mitochondriale humaine : étude de transmission de l'ADN mitochondrial lors de fécondations in vitro - caractérisation de mutations de l'ADN mitochondrial dans les maladies mitochondriales et le vieillissement musculaire." Paris 12, 2002. http://www.theses.fr/2002PA120010.
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L'ensemble de notre travail concerne trois aspects de la recherche en génétique mitochondriale humaine. Notre premier axe d'étude a été la transmission de l'ADN mitochondrial des parents aux enfants conçus par injection intracytoplasmique de spermatozoi͏̈de (ICSI). Si les risques de transmission de défauts de l'ADN nucléaire paternel sont reconnus depuis les débuts de cette technique de procréation médicalement assistée, aucune étude n'avait recherché à l'aide de techniques hautement sensibles chez les enfants conçus par ICSI la présence de molécules d'ADN mitochondrial d'origine paternelle. Nous avons montré qu'il n'existait pas, dans le sang circulant des enfants étudiés, d'ADN mitochondrial paternel détectable par les techniques utilisées. Notre deuxième axe d'étude avisé à préciser la responsabilité d'une classe de gènes de l'ADN mitochondrial, les gènes d'ARN de transfert, dans certaines maladies mitochondriales. Nous avons mis au point un outil d'analyse de l'ADN mitochondrial permettant d'analyser rapidement la séquence des 22 gènes d'ARN de transfert à la recherche de mutations de ces gènes. Appliqué à l'investigation d'une vaste cohorte de patients, cet outil a permis de détecter de très nombreuses variations de séquence, certaines déjà connues pour être pathogènes ou au contraire anodines, d'autres nouvelles et suspectes d'être pathogènes. Un travail complémentaire d'analyse des données et de validation des mutations a été nécessaire à l'interprétation des résultats. Il a également permis de mieux définir les indications d'une telle recherche. En troisième lieu, nous nous sommes intéressés à la part que pouvaient avoir les lésions de l'ADN mitochondrial dans la physiopathologie du vieillissement musculaire, et plus particulièrement dans la genèse des fibres négatives pour l'activité cytochrome oxidase. Nous avons recherché des mutations de l'ADN mitochondrial dans ces fibres, et avons pu montrer que, dans un certains nombre d'entre elles, une expansion clonale de molécules d'ADN mitochondrial porteuses de mutations ponctuelles des gènes d'ARN de transfert était responsable du déficit enzymatiqueMitochondrial genetics is important to consider when dealing with infertility, mitochondrial diseases or ageing. Our work contributes to the clarification of the role and behaviour of mitochondrial DNA (mtDNA) in those three circumstances. First, we studied mtDNA inheritance in children born after a particular in vitro fertilisation technique, i. E. Intracytoplasmic injection of spermatozoon (ICSI). Although the risk of transmission of a paternal infertility-linked nuclear defect by this technique is well known, the possible transmission of the patemal mtDNA had never been addressed by means of highly sensitive detection assays. By using different sensitive techniques, we showed that there was no detectable paternally inherited mtDNA in the peripheral blood of the 27 children who were studied. Second, we aimed at determining the contribution of mtDNA tranfer RNA (tRNA) gene defects to the pathogenesis ofmitochondrial disorders. We set up an exhaustive scanning method to screen ah tRNA genes for mutations, and applied it to a large number of selected patients with mitochondrial disorders. We found numerous sequence variations of those genes, some of them already known to be pathogenic or polymorphie, others being questionable from a functional point of view. We performed an evaluation of each questionable sequence variation by all possible means, and were able to assign a precise significance to most of them. In retrospect, we tried to delineate the best indications for the screening ofmtDNA tRNA genes. Third, we wanted to determine the contribution of mtDNA mutations to the ageing process of human muscle, at a single fibre level. We looked for large-scale rearrangements and tRNA gene point mutations in a large number of fibres defective in cytochrome c oxidase (COX- fibres) activity and an equal number of normal fibres (COX+ fibres) from normal biopsy samples taken from ageing subjects. We detected large scale rearrangements in several fibres. Most interestingly, we detected, characterised and quantified tRNA gene point mutations in several COX- fibres, such mutations being absent from COX+ fibres. We showed that clonally expanded point mutations contribute toageing process in muscle, by a segmental alteration of the respiratory chain activity
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Bertholet, Ambre. "Influence de la protéine de fusion mitochondriale OPA1 sur le métabolisme oxydatif neuronal et la transmission synaptique." Toulouse 3, 2011. http://thesesups.ups-tlse.fr/2180/.
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Depuis quelques années, de nombreux travaux suggèrent que des perturbations des fonctions mitochondriales contribuent aux maladies neurodégénératives. Les mitochondries sont particulièrement importantes pour les neurones en raison à leur rôle dans la régulation calcique, la signalisation redox, la plasticité synaptique et, in fine, la survie cellulaire. La dynamique mitochondriale contrôle la morphologie de l'organelle via un équilibre délicat entre deux forces opposées : la fusion et la fission régulées par des dynamines de la grande famille des GTPases. Notre équipe a montré que la perte ou des mutations de la protéine de fusion OPA1 entraînent des dysfonctionnements de la membrane interne mitochondriale pouvant mener à l'apoptose, qui revêtent une importance particulière dans l'atrophie optique autosomale dominante (ADOA-1). Pour comprendre les mécanismes par lesquels des altérations de la dynamique mitochondriale pourraient contribuer à des dysfonctionnements mitochondriaux et éventuellement à l'origine de la neurodégénérescence, nous avons étudié les effets de la perte d'OPA1 dans des neurones corticaux ex vivo. La perte de fonction à l'interférence à l'ARN mène à la fragmentation mitochondriale sans perturbation de la distribution mitochondriale, ni mort neuronale. Si l'arborescence dendritique est inchangée, la quantité de plusieurs protéines synaptiques est réduite, suggérant une déficience synaptique. De plus, dans ces conditions, l'état redox est altéré et la quantité protéique de complexes respiratoires spécifiques est réduite. Enfin, l'enregistrement des propriétés électrophysiologiques montrent des changements dans la transmission synaptique, notamment par une diminution de la fréquence des courants excitateurs et une augmentation de la fréquence des courants inhibiteurs. De façon intéressante, un traitement à la forskoline permet de restaurer un fonctionnement électrophysiologique normal. Pour conclure, nos données offrent de nouvelles pistes non seulement dans la compréhension de maladies neurodégénératives liées directement à la dynamique mitochondriale comme l'ADOA1, mais aussi d'autres pathologies neurodégénératives liées à un défaut du métabolisme oxydatif comme les maladies d'Alzheimer, Parkinson ou HuntingtonIn the past few years, multiple findings have suggested that disruptions of mitochondrial functions and dynamics contribute to neurodegenerative diseases. Mitochondrial functions in neurons include regulation of calcium and redox signaling, developmental and synaptic plasticity as well as the arbitration of cell survival and death. Mitochondrial dynamics controls the organelle's morphology via a delicate balance of two opposing forces: mitochondrial fusion and fission that are regulated by large dynamin-related GTPases evolutionary conserved from yeast to human. We have previously demonstrated that the fusion protein OPA1 loss or mutations led to mitochondrial inner membrane dysfunctions and apoptosis of particular importance in optic nerve pathologies like ADOA1 (autosomal dominant optic atrophy). While links emerge between defects in mitochondrial fusion and neurodegeneration, the processes involved are still largely unknown. To understand the mechanisms by which alterations of mitochondrial dynamics could contribute to mitochondria dysfunction, eventually leading to neurodegeneration, we studied the effects of OPA1 loss of function in neurons ex vivo. In cortical neurons, RNA interference of the fusion protein OPA1 led to mitochondrial fragmentation without altering neither mitochondrial distribution nor neuronal death rate. While there was no incidence on dendrites and axon size and numbers, the quantity of several synaptic proteins was reduced, suggesting synaptic impairment. In these conditions, the redox state of OPA1 depleted-neurons was impaired and specific respiratory complex proteins quantities were decreased. Finally, electrophysiological recordings showed that OPA1 depletion induced changes in synaptic transmission, particularly in decreasing of EPSC frequency and by increasing IPSC frequency. Interestingly, forskolin treatment rescue these electrophysiological defaults. In conclusion, our data may offer new insights not only into mitochondrial dynamics-linked neurodegenerative diseases like ADOA1 but to other neurodegenerative pathologies correlated with oxidative metabolism such as Huntington's, Parkinson's and Alzheimer's diseases
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Mignerot, Laure. "Caractérisation cellulaire et génétique de la parthénogenèse chez l’algue brune Ectocarpus sp." Electronic Thesis or Diss., Sorbonne université, 2018. http://www.theses.fr/2018SORUS621.
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Bien que la reproduction sexuée soit prédominante chez les eucaryotes, plusieurs centaines d’organismes ont opéré une transition vers la reproduction asexuée. Les transitions entre reproduction sexuée et asexuée peuvent avoir une importance et des conséquences évolutives mais elles restent largement peu décrites au niveau écologique, moléculaire, génétique ou cytologique. La reproduction asexuée par parthénogenèse correspond au développement d’un organisme à partir de gamètes sans fécondation. Bien que beaucoup d’eucaryotes soient parthénogénétiques, nous connaissons très peu les bases génétiques, les causes et les conséquences évolutives conduisant à ce mode de reproduction asexuée. Les algues brunes sont un groupe d’eucaryotes multicellulaires qui présentent une incroyable diversité en termes de cycle de vie, de systèmes sexués ou mode de reproduction. Elles représentent d’excellents modèles pour étudier l’origine, l’évolution et les mécanismes de la parthénogenèse. Dans cette thèse, les nombreux outils génétiques et cellulaires développés pour l’algue brune modèle Ectocarpus ont permis de caractériser les loci impliqués dans la parthénogenèse et de mettre en lumière les causes et les conséquences de ce développement à l’échelle de l’organisme. Nos résultats soulignent le rôle clé des chromosomes sexuels en tant que régulateur majeur de la reproduction asexuée, ainsi que deux loci autosomaux. Des effets négatifs de la parthénogenèse sur la fitness des mâles ont été identifiés ainsi que des effets sur la fitness des générations du cycle de vie. Ces résultats indiquent que la parthénogenèse pourrait être à la fois sous sélection sexuelle et sous sélection antagoniste par rapport aux générations (polyploidallie) (Chapitre 2). La croissance des zygotes est significativement affectée par la capacité parthénogénétique des parents mâles et la transmission des mitochondries a été suivie afin de caractériser les retards de croissances observés (Chapitre 2 et 3). En parallèle, la transmission mitochondriale chez Ectocarpus sp.7 s’est révélé être non usuelle (Chapitre 3). Enfin, la carte génétique générée (Chapitre 2) pour l’espèce Ectocarpus siliculosus a été comparée à celle d’Ectocarpus sp.7 (génome de référence séquencé en 2010) et a révélé une synténie fortement conservé entre les deux espèces (Chapitre 4). En étudiant la parthénogenèse chez un organisme multicellulaire qui a évolué indépendamment des plantes et des animaux, ce travail a participé à approfondir les connaissances sur les mécanismes évolutifs conduisant à la parthénogenèseAlthough sexual reproduction predominates in eukaryotes, several hundred lineages have undergone the transition from sexuality to asexuality. Transitions between sexual and asexual reproduction are believed to have important evolutionary and ecological consequences, yet the molecular, genetic, and cytological foundations of such transitions remain elusive. One type of asexual reproduction is parthenogenesis, i.e., the development of an adult organism directly from gametes in the absence of fertilisation. Although many eukaryotes are capable of reproducing by parthenogenesis, we know very little about its genetic basis, and the evolutionary causes and consequences of transitions to asexuality are poorly understood. The brown algae are a group of multicellular eukaryotes, that show an extraordinary diversity of types of life cycle, sexual systems, modes of reproduction, and they provide excellent models to look at the origins, evolution and mechanisms underlying parthenogenesis. In this thesis, we have used a wide array of genomic and cell biology tools available for the model brown alga Ectocarpus to identify and characterize loci involved in parthenogenesis, shedding light on the causes and consequences of parthenogenesis at the organism level. Our results highlight the key role of the sex chromosome as a major regulator of asexual reproduction, together with two autosomal loci. Importantly, we identify several negative effects of parthenogenesis on male fitness, but also different fitness effects between parthenogenesis and life cycle generations, supporting the idea that parthenogenesis may be under both sexual selection and generation/ploidally-antagonistic selection (Chapter 2). Zygotic growth was significantly affected by the parthenogenetic capacity of the male parent and the putative role of mitochondrial inheritance patterns on the fitness of sporophytes was also investigated (Chapter 2 and 3). This work revealed an unusual transmission pattern of mitochondria specifically in Ectocarpus species 7 (Chapter 3). Finally, the QTL analysis (Chapter 2) required the construction of a genetic map for Ectocarpus siliculosus and a comparison with Ectocarpus species 7 genetic map (reference genome sequenced in 2010) showed that the synteny was highly conserved between the two species (Chapter 4). By investigating parthenogenesis in a multicellular organism that has independently evolved from plants and animals, the work presented in this thesis has helped to assess the diversity of evolutionary mechanisms that lead to parthenogenesis
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Haars, Jonathan. "Inheritance patterns of mitochondrial DNA in Drosophila paulistorum: substantial paternal transmission and the possible role of mitochondria in speciation." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-382016.
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Direct studies of speciation are possible in the superspecies complex of Drosophila paulistorum, which consists of six different semispecies undergoing incipient speciation. Strict maternal inheritance of mitochondria is the most common pattern of mitochondrial inheritance in animals. Here I show that paternal transmission of mitochondrial DNA occurs in the heteroplasmic Orinocan semispecies and is not limited to hybrid offspring. Inheritance of one mitotype is mainly maternal while the other is mainly paternal; a highly unusual pattern of mitochondrial inheritance. I used absolute quantification real-time PCR on DNA extracted from eggs and imagoes from the Amazonian and Orinocan semispecies, as well as hybrids between these two semispecies. In crosses performed between F1 hybrids with a combination of mitotypes not found in any of the parents, no F2 hybrids were acquired. One possible explanation for this is that differences in mitotypes and inheritance patterns of mitochondrial DNA may cause incompatibilities between the genomes of D. paulistorum. This may be one cause of hybrid inviability and genetic isolation between semispecies, a necessary part of the speciation process. This further complicates the story of the ongoing speciation process in the D. paulistorum superspecies complex, which offers much to learn about speciation, mitochondrial inheritance and interactions between multiple genomes in the same organism.
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Wai, Timothy. "Germline transmission of mitochondrial DNA in the mouse." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40735.
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In mammals, mitochondria and mitochondrial DNA (mtDNA) are transmitted through the female germline. Mature oocytes contain nearly 200,000 copies of mtDNA, organized at 1-2 copies per organelle. Despite the high genome copy number, mtDNA sequence variants are observed to segregate rapidly between generations, and this has led to the concept of a genetic bottleneck for the transmission of mtDNA. In this thesis, I demonstrate that a subgroup of replicating genomes in the early post-natal ovary is responsible for the rapid segregation of mtDNA. I show that the rate of segregation of mtDNA can be accelerated when mtDNA copy number is further reduced in heteroplasmic germline-specific knockout mouse models, yet very extreme reductions in germ cell mtDNA content seem to cause female-specific infertility. Low copy number embryos can be fertilized and proceed through preimplantation development yet fail to develop normally after implantation. Tracking the developmental outcome of embryos containing a range of mtDNAs points to a developmental threshold of about 50,000 copies of mtDNA in the oocyte In this thesis I advance the hypothesis that the large number of mitochondria and mtDNAs present in the oocyte represent a genetic mechanism to ensure their distribution to the gametes and somatic cells of the next generation. If true, mtDNA copy number may be the most important determinant of oocyte quality not because of the effects on oocyte metabolism, but because too few would result in a maldistribution in the embryo.Les mitochondries et l’ADN mitochondrial (ADNmt) sont des organites cellulaires qui ne sont transmis que par l'ovule de la mère. Chez les mammifères, l’ovocyte contient presque 200 000 copies d’ADNmt, avec 1-2 copies au sein de chaque mitochondrie. Malgré la grande quantité d’ADNmt, nous observons une ségrégation rapide des variants de séquences entre les générations qui nous amène à l’hypothèse d’un goulot d’étranglement génétique pour l’ADNmt. Par cette thèse, je démontre que ce phénomène est dû à un sous-groupe de génomes mitochondriaux qui se multiplient dans l’ovocyte postnatal de la souris. En outre, je démontre qu’une réduction d’ADNmt dans les cellules de souche germinale peut augmenter la vitesse à laquelle ces génotypes se séparent. Une très importante réduction d’ADNmt dans les ovocytes de ces souris mutantes les rend stériles. Or la fertilisation de ces ovocytes ainsi que le développement pré-implantatoire se déroulent normalement, par contre l’embryon qui provient d’un ovocyte avec une très faible quantité d’ADNmt ne peut compléter son développement post-implantatoire. Par cette thèse, je propose l’hypothèse suivante : que la grande quantité de mitochondries et génomes mitochondriaux sert à distribuer un nombre suffisant de ces organites aux cellules somatiques et germinales de la prochaine génération. Si cela est vrai, la quantité d’ADNmt pourrait être le plus important déterminant quant à la qualité de l’ovocyte, pas à cause de ses effets sur le métabolisme de l’ovocyte, mais par le fait qu’une quantité insuffisante empêcherait sa distribution dans les cellules de l’embryon.
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Gooding, Christopher Michael. "Mitochondrial DNA replication and transmission in Saccharomyces cerevisiae." Thesis, University of Hertfordshire, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303447.
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Vaccaro, V. "The role of presynaptic mitochondria in neuronal transmission and plasticity." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1468434/.
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Mitochondria are essential for cellular processes such as energy provision and Ca2 + buffering. Due to the highly polarized architecture of neurons, the positioning of mitochondria to areas of high activity is crucial for normal neuronal function. It has previously been shown that mitochondria are trafficked dependent upon neuronal activity. In this thesis, the role of mitochondria at the presynaptic terminal is investigated in order to determine whether the presence of mitochondria in turn influences neuronal transmission. Dual-colour live imaging reveals that terminals occupied by a mitochondrion show lower Ca2 + responses and that transmitter release is reduced. Furthermore, evidence for a role of activity-dependent positioning of mitochondria in homeostatic plasticity is shown, which is dependent upon the function of the Ca2 + -sensitive mitochondrial protein Miro1. Furthermore, the role of Miro1 in positioning mitochondria at presynaptic terminals is investigated in a knockout mouse system. This shows that calcium buffering seems to be changed in the Miro1 knockout neurons and that activity-dependent positioning of mitochondria to presynaptic terminals is affected. Taken together, this thesis examines the functions of mitochondria in the presynaptic terminal and sheds light on how their presence in the terminal may be regulated.
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Lloyd, Rhiannon Eleanor Iris. "The regulation of mitochondrial DNA transmission to generate offspring that are genetically identical." Thesis, University of Birmingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433521.
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Donor cell mitochondrial DNA (D-mtDNA) outcomes in somatic cell nuclear transfer (SCNT)-embryos, foetuses and offspring are variable. The factors that regulate D-mtDNA transmission and its influence ,post-SCNT are uncertain. Therefore, ovine primary foetal fibroblast (PDFF2 and SSFl) cells were depleted of their mtDNA to varying degrees using low concentrations of ethidium bromide. JC 1 staining, transmission electron microscopy, reverse transcription PCR, immunocytochemistry and Western blotting were used to determine the effects of mtDNA-depletion on the ovine cells prior to SCNT. PDFF2 cells containing full (PDFF2 mtDNA), partially-depleted (PDFF2 mtDNAPD ) and almost completely depleted (PDFF2 mtDNA 0) mtDNA complements were used successfully to produce SCNT -embryos up to the hatched blastocyst stage. Quantitative allele-specific-real time PCR analysis revealed that 74% of the PDFF2 SCNT-embryos contained D-mtDNA (range 0.01 to 8.72%). Furthermore, the persistence (P < 0.002) and amount of D-mtDNA (P < 0.007) was significantly reduced in PDFF2 mtDNA 0 embryos compared to PDFF2 mtDNA+ embryos, although their blastocyst formation rates and number of cell per blastocyst were similar. In order to verify the PDFF2 SCNT-embryo outcomes, another set of SCNTembryos was produced using SSFI cells ~ontaining full (SSFI mtDNA+) and almost completely depleted (SSFI mtDNAo) mtDNA complements. 86% of the SSFI SCNT-embryos contained D-mtDNA (range 0.01 to 1.19%) and the amount ofD-mtDNA was reduced, though not significantly, in the SSFI mtDNAo embryos compared to the SSFI mtDNA + embryos. Interestingly, the SSFI mtDNA 0 blastocysts contained significantly more cells than SSFI mtDNA+ blastocysts (P < 0.05). Taken together, these data show that: I) persistent D-mtDNA is a common feature following ovine SCNT; 2) D-mtDNA outcomes in ovine SCNT -embryos are influenced by the amount of mtDNA in the nuclear donor cells, 3) small amounts of D-mtDNA « 9%) in ovine SCNT-embryos do not influence their blastocyst formation rates, and finally 4) depending on the cell line, using nuclear donors almost completely depleted ofmtDNA increases ovine SCNT -blastocyst cell number and therefore could enhance their developmental competence.
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Sullins, Jennifer Anne. "Accumulation and Transmission Dynamics of a Naturally-Occurring mtDNA Deletion in Caenorhabditis briggsae." PDXScholar, 2018. https://pdxscholar.library.pdx.edu/open_access_etds/4729.
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Maintaining mitochondrial genome sequence integrity is essential for preserving normal mitochondrial function. Several human diseases have been associated with heteroplasmic mitochondrial genome mutations, but few genetic systems can simultaneously represent pathogenic mitochondrial genome evolution and inheritance. The nematode Caenorhabditis briggsae is one such model. Natural C. briggsae isolates are globally-distributed and phylogenetically grouped into three distinct clades, with isolates exhibiting varying levels of a large-scale mtDNA deletion, nad5∆. Furthermore, a small subset of clade II isolates exhibits putative compensatory mutations that may reduce the risk of deletion formation and accumulation in those populations. In this thesis, the author characterizes the dynamics of nad5∆ heteroplasmy levels during both development and transmission in several C. briggsae natural isolates, including two containing putatively protective compensatory mutations (C+).
For all isolates tested, nad5∆ heteroplasmy levels increased across nematode development, with L1 (first larval stage) exhibiting the lowest deletion load for all but one isolate that exhibited highly variable nad5∆ levels, while the increase was slowest and overall nad5∆ levels remained relatively low in C+ isolates. These results support previous work suggesting that nad5∆ is a selfish element and demonstrate the protective nature of compensatory mutations in inhibiting mtDNA deletion accumulation.
In nad5∆ inheritance assays, C+ isolates displayed a strong pattern of reversion to wildtype mtDNA levels that was not seen in isolates lacking compensatory mutations (C-). These assays also showed that nad5∆ inheritance was not well predicted by total maternal nad5∆ proportion in either C+ or C- isolates; offspring nad5∆ levels were generally much lower than maternal levels, consistent with some form of negative selection operating between generations. Assays of both maternal somatic and gonadal tissues had slightly more power to predict offspring deletion levels than did assays of whole-worm maternal samples; this result likely points to variance in deletion levels originating from an untested parental tissue type present within the whole-worm samples.
This thesis provided deeper insights into the patterns of mtDNA deletion transmission and age-associated dynamics. It was the first project of its type to survey mutation dynamics and heteroplasmy levels of a naturally-occurring large-scale mtDNA deletion. Thus, this work serves to further develop C. briggsae for use as an experimental model of human mtDNA deletion dynamics and mitochondrial dysfunction.
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Chat, Joelle Catherine. "Transmission des génomes cytoplasmiques et phylogénie moléculaire chez Actinidia." Paris, Institut national d'agronomie de Paris Grignon, 2003. http://www.theses.fr/2003INAP0006.
Full textBooks on the topic "Transmission mitochondriale"
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Kang, Eunji Ellen. Effects of mitochondrial dysfunction on synaptic transmission in rat hippocampal slices. 2005.
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Hill, Geoffrey E. Mitonuclear Ecology. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198818250.001.0001.
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Eukaryotes were born of a chimeric union of two prokaryotes. The legacy of this fusion is organisms with both a nuclear and mitochondrial genome that must work in a coordinated fashion to enable cellular respiration. The coexistence of two genomes in a single organism requires tight coadaptation to enable function. The need for coadaptation, the challenge of co-transmission, and the possibility of genomic conflict between mitochondrial and nuclear genes have profound consequences for the ecology and evolution of eukaryotic life. This book defines mitonuclear ecology as an emerging field that reassesses core concepts in evolutionary ecology in light of the necessity of mitonuclear coadaptation. I discuss and summarize research that tests new mitonuclear-based theories for the evolution of sex, two sexes, senescence, a sequestered germ line, speciation, sexual selection, and adaptation. The ideas presented in this book represent a paradigm shift for evolutionary ecology. Through the twentieth century, mitochondrial genomes were dismissed as unimportant to the evolution of complex life because variation within mitochondrial genomes was proposed to be functionally neutral. These conceptions about mitochondrial genomes and mitonuclear genomic interactions have been changing rapidly, and a growing literature in top journals is making it increasingly clear that the interactions of the mitochondrial and nuclear genomes over the past 2 billion years have played a major role in shaping the evolution of eukaryotes. These new hypotheses for the evolution of quintessential characteristics of complex life hold the potential to fundamentally reshape the field of evolutionary ecology and to inform the emerging fields of mitochondrial medicine and mitochondrial-based reproductive therapies.
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Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Genetics. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0010.
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Chapter 10 covers the basic science and clinical topics relating to genetics which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers karyotype, mitosis, and meiosis, mechanisms of inheritance/disease transmission, mitochondrial disease, trinucleotide repeats and imprinting, investigative techniques in genetic medicine, Down syndrome, Klinefelter syndrome, Turner syndrome, neurofibromatosis, tuberous sclerosis, myotonic dystrophy, Friedreich ataxia, fragile X syndrome, Prader-Willi syndrome, Angelman syndrome, and Ehlers-Danlos syndrome.
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Gaitanis, John, Phillip L. Pearl, and Howard Goodkin. The EEG in Degenerative Disorders of the Central Nervous System. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0013.
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Nervous system alterations can occur at any stage of prenatal or postnatal development. Any of these derangements, whether environmental or genetic, will affect electrical transmission, causing electroencephalogram (EEG) alteration and possibly epilepsy. Genetic insults may be multisystemic (for example, neurocutaneous syndromes) or affect only the brain. Gene mutations account for inborn errors of metabolism, channelopathies, brain malformations, and impaired synaptogenesis. Inborn errors of metabolism cause seizures and EEG abnormalities through a variety of mechanisms, including disrupted energy metabolism (mitochondrial disorders, glucose transporter defect), neuronal toxicity (amino and organic acidopathies), impaired neuronal function (lysosomal and peroxisomal disorders), alteration of neurotransmitter systems (nonketotic hyperglycinemia), and vitamin and co-factor dependency (pyridoxine-dependent seizures). Environmental causes of perinatal brain injury often result in motor or intellectual impairment (cerebral palsy). Multiple proposed etiologies exist for autism, many focusing on synaptic development. This chapter reviews the EEG findings associated with this myriad of pathologies occurring in childhood.
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Benarroch, Eduardo E. Neuroscience for Clinicians. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.001.0001.
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The aim of this book is to provide the clinician with a comprehensive and clinical relevant survey of emerging concepts on the organization and function of the nervous system and neurologic disease mechanisms, at the molecular, cellular, and system levels. The content of is based on the review of information obtained from recent advances in genetic, molecular, and cell biology techniques; electrophysiological recordings; brain mapping; and mouse models, emphasizing the clinical and possible therapeutic implications. Many chapters of this book contain information that will be relevant not only to clinical neurologists but also to psychiatrists and physical therapists. The scope includes the mechanisms and abnormalities of DNA/RNA metabolism, proteostasis, vesicular biogenesis, and axonal transport and mechanisms of neurodegeneration; the role of the mitochondria in cell function and death mechanisms; ion channels, neurotransmission and mechanisms of channelopathies and synaptopathies; the functions of astrocytes, oligodendrocytes, and microglia and their involvement in disease; the local circuits and synaptic interactions at the level of the cerebral cortex, thalamus, basal ganglia, cerebellum, brainstem, and spinal cord transmission regulating sensory processing, behavioral state, and motor functions; the peripheral and central mechanisms of pain and homeostasis; and networks involved in emotion, memory, language, and executive function.
Book chapters on the topic "Transmission mitochondriale"
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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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Allen, Carol A., Mark Van Der Giezen, and John F. Allen. "Origin, Function, and Transmission of Mitochondria." In Origin of Mitochondria and Hydrogenosomes, 39–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-38502-8_3.
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Brdiczka, Dieter, Volker Adams, Matthias Kottke, and Roland Benz. "Topology of Peripheral Kinases: its Importance in Transmission of Mitochondrial Energy." In Anion Carriers of Mitochondrial Membranes, 361–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74539-3_30.
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Srirattana, Kanokwan, and Justin C. St. John. "Transmission of Dysfunctional Mitochondrial DNA and Its Implications for Mammalian Reproduction." In Cellular and Molecular Basis of Mitochondrial Inheritance, 75–103. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/102_2018_3.
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Sánchez-Calabuig, María Jesús, Noelia Fonseca Balvís, Serafín Pérez-Cerezales, and Pablo Bermejo-Álvarez. "Reproductive Approaches to Prevent the Transmission of Mitochondrial Diseases." In Mechanisms Linking Aging, Diseases and Biological Age Estimation, 217–26. Boca Raton, FL : CRC Press, 2016. | “A science publishers book.”: CRC Press, 2017. http://dx.doi.org/10.1201/9781315371382-24.
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Hyslop, Louise. "Assisted Reproductive Technologies to Prevent Transmission of Mitochondrial DNA Disease." In In Vitro Fertilization, 861–67. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-43011-9_72.
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Miyamoto, Kiyoshi, and Keiichiro Yamaguchi. "Numerical Density, Estimation of Mitochondria in Thick Slice by Transmission Electron Microscopy." In Science on Form, 517–25. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-3757-4_60.
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John, Justin C. St, and Keith H. S. Campbell. "The Consequences of Reprogramming a Somatic Cell for Mitochondrial DNA Transmission, Inheritance and Replication." In Nuclear Reprogramming and Stem Cells, 83–97. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-225-0_8.
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Hill, Geoffrey E. "Coevolution, co-transmission, and conflict." In Mitonuclear Ecology, 77–95. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198818250.003.0004.
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Mitochondrial genes and nuclear genes are replicated and transmitted across generations as physically separated units. The extent to which these autonomous genomes are co-transmitted depends on the position of nuclear genes on autosomes versus sex chromosomes, and co-transmission has important implications for mitonuclear coevolution and conflict. Mitonuclear co-transmission, coadaptation, and coevolution are potentially very important for understanding fundamental evolutionary phenomena like Haldane’s rule. In addition, because mitochondrial genomes are transmitted strictly through maternal lines in most eukaryotes, selection on mitochondrial genes can favor female fitness over male fitness, leading to mother’s curse. The chapter assesses and draws conclusions about the relative importance of mitonuclear coadaptation and conflict in the evolution of eukaryotic lineages.
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Tembe, Sanket. "Maneuvering Mitochondria for Better Understanding of Therapeutic Potential of mtDNA Mutation." In Mitochondrial Diseases [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96915.
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Heterogeneity of mitochondrial diseases in terms of genetic etiology and clinical management makes their diagnosis challenging. Mitochondrial genome, basic mitochondrial genetics, common mutations, and their correlation with human diseases is well-established now and advances in sequencing is accelerating the molecular diagnostics of mitochondrial diseases. Major research focus now is on development of mtDNA intervention techniques like mtDNA gene editing, transfer of exogenous genes (sometimes even entire mtDNA) that would compensate for mtDNA mutations responsible for mitochondrial dysfunction. Although these genetic manipulation techniques have good potential for treatment of mtDNA diseases, research on such mitochondrial manipulation fosters ethical issues. The present chapter starts with an introduction to the factors that influence the clinical features of mitochondrial diseases. Advancement in treatments for mitochondrial diseases are then discussed followed by a note on methods for preventing transmission of these diseases.
Conference papers on the topic "Transmission mitochondriale"
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Pinzetta, Giulia, Nicole Bernd Becker, Felipe Krimberg, Ângela Zanatta, Laura Siqueira, Gabriele Zanirati, Jaderson Costa da Costa, and Daniel Marinowic. "Effects of ZIKV + IgG+ complex on murine microglial cells." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.562.
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Background: Infection by Zika virus (ZIKV) is associated with damage to the Central Nervous System, such as Congenital Zika Syndrome1 . Due to its transplacental transmission, ZIKV induces neuroinflammation and microglial activation, resulting in lesions that can compromise neurodevelopment2-4. The fetus protection can be provided by maternal antibodies. However, this protection is still controversial5 . In this context, it is necessary to elucidate the effects of ZIKV and the mechanisms involved. Objectives: The present work aim to evaluate the role of the ZIKV+IgG+ complex in murine microglia cells (BV2). Design and setting: BV2 were exposed for 24 or 72 hours, to ZIKV, ZIKA-IgG+ or ZIKV+IgG+ complex. Methods: Effects of exposure to treatments were evaluated by MTT, oxidation of DCFHDA (ROS production)6 and mitochondrial membrane potential (Δ∴ϑ), measured by JC-17 assay. Results: It was observed that ZIKV-IgG+ and the ZIKV+IgG+ complex are cytotoxic to microglia, impairing the viability of these cells, altering Δ∴ϑ and inducing the production of ROS, especially in long-term exposure8,9. Negative action mediated by these antibodies may be a result of oxidative stress and a intervention in the Δ∴ϑ. Conclusion: ZIKV-IgG+ antibodies are harmful to microglia and these mechanisms may be related to the potential for ZIKV neuroinflammation.
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Carter, G., and J. B. Gavin. "THE EFFECTS OF ISCHAEMIC METABOLITES ON THE ENDOCARDIAL ENDOTHELIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643355.
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Although mural thrombosis is an important complication of myocardial infarction, little is known of the mechanisms by which death of underlying myocytes initiates thrombus fooiation cm the endocardiim. The sequence of morphological changes which develop in the endocardiim when exposed to ischaemic metabolites was determined in isolated beating rat hearts perfused with oxygenated Krebs-Henseleit buffer (KHB). Lactate (pH7.4), hydrogen ions (HC1, pH6.4) and lactic acid (pH6.4) were passed through a two-way concentric catheter ligated into the left ventricles for periods of 1,2,4,6 and 8 hours (n=4 in each group). Ventricles were then flushed with KHB, fixed in 2.5% glutaraldehyde and examined by scanning and transmission electron microscopy. The morphological changes observed wene qualitatively similar following the infusion of each solution, and all changes increased in severity and extent from one to four hours exposure. Quantitatively the most severe changes were observed with lactic acid. After one hour exposure to lactic acid 3.16 ± 2.35% of the endothelial cells on the papillary muscle showed separation and 7.85 ± 2.44% of cells had exfoliated exposing the basal lamina and after four hours 6.68 ± 2.0% of cells had separated and 16.05 ± 2.67% had been lost. Some exposed connective tissue fibres were evident after one hour (0.94 ± 1.19% of surface area exposed) and the smooth basal lamina had been lost from 4.67 ± 1.04% of the surface with subsequent exposure of the connective tissue after four hours. In all groups mitochondria of endothelial cells were swollen, their matrix electron-lucent and their cristae distorted and fragmented; the endoplasmic reticulun was diluted; and chromatin of nuclei was marginated and clmped (H+ ions and lactic acid only). Superficial myocytes showed similar changes. Electron dense inclusions were also observed in the mitochondria of myocytes exposed to hydrogen ions and lactic acid. Thus perfusion of the ventricle with ischaemic metabolites, which could diffuse from an infarct in vivo, can cause substantial damage to the endocardial endothelium.Research supported by the Medical Research Council of New Zealand
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Kim, Dong Sik. "Intensity compensation of the mitochondria tilted image sequence obtained from the transmission electron microscopy." In 2009 16th IEEE International Conference on Image Processing (ICIP 2009). IEEE, 2009. http://dx.doi.org/10.1109/icip.2009.5414557.
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Frojmovic, Mony M., Truman Wong, Jane Wylie, and J. G. White. "PLATELET EXTERNAL SURFACE MEMBRANE IS OSMOTICALLY DOUBLED IRRESPECTIVE OF SIZE OR SPECIES (HUMAN/BOVINE): DYNAMICS AND MEMBRANE SOURCES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643905.
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Osmotic swelling can double the external plasma membrane surface area of human platelets independently of size, proposed to recruit the open surface-connected canalicular system ((SCCS) (Thrombos. Res. Suppl. VI: 119, 1986). As bovine (B) platelets have been reported to lack SCCS, we compared osmotic swelling for B and human (H) cells. Addition of water to piatelet-rich-plasma (10-90% v/v) caused sequential shape change and osmotic spherocyte (OS) formation, analyzed for size and surface area changes from time-dependent phase-contrast videomicroscopic images. Selected samples were fixed and stained with tannic acid prior to osmic acid fixation for visualization of open SCCS by transmission electron microscopy. B platelets required 3-4x less water dilution of PRP than H platelets, with significant OS forming at 20% water addition. Continued water dilution converted 50% of platelets to OS, with maximally stable swelling and no significant lysis for bovine OS up to 60% dilution. Electron micrographs of unactivated discocytes (D) and of optimally-swollen OS showed open SCCS in human D not detectable in any of the swollen platelets, though granules, mitochondria and a small number of vesicles and vacuoles persisted; no evidence for any open SCCS was found for bovine D or OS, though the OS otherwise appeared similar to H-0S. Geometric measurements of D and nonlysed OS showed a stable, maximal 2.1±0.1 fold increase in external plasma membrane surface area with osmotic swelling, identical for different-sized H platelets (mean volume = 2.8-6.8 f1) or for B platelets (3.6 f1 ). B platelets show equal or greater sensitivity for ADP-induced activation as H platelets, with 2-fold slower maximal rates of recruitment in early aggregation. As osmotic swelling appears to primarily externalize SCCS in H platelets, the identical relative amounts of internal membrane externalized for B platelets is hypothesized to arise from an osmotically more labile, “closed”, and structurally simpler SCCS or from a distinct membrane source tnan in H platelets.