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Relevant bibliographies by topics / Mitochondrial biogenesis and quality control

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Academic literature on the topic 'Mitochondrial biogenesis and quality control'

Author: Grafiati

Published: 6 September 2023

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Journal articles on the topic "Mitochondrial biogenesis and quality control"

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Hernando-Rodríguez, Blanca, and Marta Artal-Sanz. "Mitochondrial Quality Control Mechanisms and the PHB (Prohibitin) Complex." Cells 7, no. 12 (November 29, 2018): 238. http://dx.doi.org/10.3390/cells7120238.

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Mitochondrial functions are essential for life, critical for development, maintenance of stem cells, adaptation to physiological changes, responses to stress, and aging. The complexity of mitochondrial biogenesis requires coordinated nuclear and mitochondrial gene expression, owing to the need of stoichiometrically assemble the oxidative phosphorylation (OXPHOS) system for ATP production. It requires, in addition, the import of a large number of proteins from the cytosol to keep optimal mitochondrial function and metabolism. Moreover, mitochondria require lipid supply for membrane biogenesis, while it is itself essential for the synthesis of membrane lipids. To achieve mitochondrial homeostasis, multiple mechanisms of quality control have evolved to ensure that mitochondrial function meets cell, tissue, and organismal demands. Herein, we give an overview of mitochondrial mechanisms that are activated in response to stress, including mitochondrial dynamics, mitophagy and the mitochondrial unfolded protein response (UPRmt). We then discuss the role of these stress responses in aging, with particular focus on Caenorhabditis elegans. Finally, we review observations that point to the mitochondrial prohibitin (PHB) complex as a key player in mitochondrial homeostasis, being essential for mitochondrial biogenesis and degradation, and responding to mitochondrial stress. Understanding how mitochondria responds to stress and how such responses are regulated is pivotal to combat aging and disease.

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Gottlieb, Roberta A., Honit Piplani, Jon Sin, Savannah Sawaged, Syed M. Hamid, David J. Taylor, and Juliana de Freitas Germano. "At the heart of mitochondrial quality control: many roads to the top." Cellular and Molecular Life Sciences 78, no. 8 (February 5, 2021): 3791–801. http://dx.doi.org/10.1007/s00018-021-03772-3.

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AbstractMitochondrial quality control depends upon selective elimination of damaged mitochondria, replacement by mitochondrial biogenesis, redistribution of mitochondrial components across the network by fusion, and segregation of damaged mitochondria by fission prior to mitophagy. In this review, we focus on mitochondrial dynamics (fusion/fission), mitophagy, and other mechanisms supporting mitochondrial quality control including maintenance of mtDNA and the mitochondrial unfolded protein response, particularly in the context of the heart.

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Halling, Jens Frey, and Henriette Pilegaard. "PGC-1α-mediated regulation of mitochondrial function and physiological implications." Applied Physiology, Nutrition, and Metabolism 45, no. 9 (September 2020): 927–36. http://dx.doi.org/10.1139/apnm-2020-0005.

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The majority of human energy metabolism occurs in skeletal muscle mitochondria emphasizing the importance of understanding the regulation of myocellular mitochondrial function. The transcriptional co-activator peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) has been characterized as a major factor in the transcriptional control of several mitochondrial components. Thus, PGC-1α is often described as a master regulator of mitochondrial biogenesis as well as a central player in regulating the antioxidant defense. However, accumulating evidence suggests that PGC-1α is also involved in the complex regulation of mitochondrial quality beyond biogenesis, which includes mitochondrial network dynamics and autophagic removal of damaged mitochondria. In addition, mitochondrial reactive oxygen species production has been suggested to regulate skeletal muscle insulin sensitivity, which may also be influenced by PGC-1α. This review aims to highlight the current evidence for PGC-1α-mediated regulation of skeletal muscle mitochondrial function beyond the effects on mitochondrial biogenesis as well as the potential PGC-1α-related impact on insulin-stimulated glucose uptake in skeletal muscle. Novelty PGC-1α regulates mitochondrial biogenesis but also has effects on mitochondrial functions beyond biogenesis. Mitochondrial quality control mechanisms, including fission, fusion, and mitophagy, are regulated by PGC-1α. PGC-1α-mediated regulation of mitochondrial quality may affect age-related mitochondrial dysfunction and insulin sensitivity.

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Mtango, N. R., A. J. Harvey, K. E. Latham, and C. A. Brenner. "Molecular control of mitochondrial function in developing rhesus monkey oocytes and preimplantation-stage embryos." Reproduction, Fertility and Development 20, no. 7 (2008): 846. http://dx.doi.org/10.1071/rd08078.

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The mitochondrion undergoes significant functional and structural changes, as well as an increase in number, during preimplantation embryonic development. The mitochondrion generates ATP and regulates a range of cellular processes, such as signal transduction and apoptosis. Therefore, mitochondria contribute to overall oocyte quality and embryo developmental competence. The present study identified, for the first time, the detailed temporal expression of mRNAs related to mitochondrial biogenesis in rhesus monkey oocytes and embryos. Persistent expression of maternally encoded mRNAs was observed, in combination with transcriptional activation and mRNA accumulation at the eight-cell stage, around the time of embryonic genome activation. The expression of these transcripts was significantly altered in oocytes and embryos with reduced developmental potential. In these embryos, most maternally encoded transcripts were precociously depleted. Embryo culture and specific culture media affected the expression of some of these transcripts, including a deficiency in the expression of key transcriptional regulators. Several genes involved in regulating mitochondrial transcription and replication are similarly affected by in vitro conditions and their downregulation may be instrumental in maintaining the mRNA profiles of mitochondrially encoded genes observed in the present study. These data support the hypothesis that the molecular control of mitochondrial biogenesis, and therefore mitochondrial function, is impaired in in vitro-cultured embryos. These results highlight the need for additional studies in human and non-human primate model species to determine how mitochondrial biogenesis can be altered by oocyte and embryo manipulation protocols and whether this affects physiological function in progeny.

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Huang, Jia, Ruibing Li, and Chengbin Wang. "The Role of Mitochondrial Quality Control in Cardiac Ischemia/Reperfusion Injury." Oxidative Medicine and Cellular Longevity 2021 (June 9, 2021): 1–13. http://dx.doi.org/10.1155/2021/5543452.

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A healthy mitochondrial network produces a large amount of ATP and biosynthetic intermediates to provide sufficient energy for myocardium and maintain normal cell metabolism. Mitochondria form a dynamic and interconnected network involved in various cellular metabolic signaling pathways. As mitochondria are damaged, controlling mitochondrial quantity and quality is activated by changing their morphology and tube network structure, mitophagy, and biogenesis to replenish a healthy mitochondrial network to preserve cell function. There is no doubt that mitochondrial dysfunction has become a key factor in many diseases. Ischemia/reperfusion (IR) injury is a pathological manifestation of various heart diseases. Cardiac ischemia causes temporary tissue and organelle damage. Although reperfusion is essential to compensate for nutrient deficiency, blood flow restoration inconsequently further kills the previously ischemic cardiomyocytes. To date, dysfunctional mitochondria and disturbed mitochondrial quality control have been identified as critical IR injury mechanisms. Many researchers have detected abnormal mitochondrial morphology and mitophagy, as well as aberrant levels and activity of mitochondrial biogenesis factors in the IR injury model. Although mitochondrial damage is well-known in myocardial IR injury, the causal relationship between abnormal mitochondrial quality control and IR injury has not been established. This review briefly describes the molecular mechanisms of mitochondrial quality control, summarizes our current understanding of the complex role of mitochondrial quality control in IR injury, and finally speculates on the possibility of targeted control of mitochondria and the methods available to mitigate IR injury.

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Kim, Yuho, Matthew Triolo, and David A. Hood. "Impact of Aging and Exercise on Mitochondrial Quality Control in Skeletal Muscle." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–16. http://dx.doi.org/10.1155/2017/3165396.

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Mitochondria are characterized by its pivotal roles in managing energy production, reactive oxygen species, and calcium, whose aging-related structural and functional deteriorations are observed in aging muscle. Although it is still unclear how aging alters mitochondrial quality and quantity in skeletal muscle, dysregulation of mitochondrial biogenesis and dynamic controls has been suggested as key players for that. In this paper, we summarize current understandings on how aging regulates muscle mitochondrial biogenesis, while focusing on transcriptional regulations including PGC-1α, AMPK, p53, mtDNA, and Tfam. Further, we review current findings on the muscle mitochondrial dynamic systems in aging muscle: fusion/fission, autophagy/mitophagy, and protein import. Next, we also discuss how endurance and resistance exercises impact on the mitochondrial quality controls in aging muscle, suggesting possible effective exercise strategies to improve/maintain mitochondrial health.

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Roque, Willy, Karina Cuevas-Mora, and Freddy Romero. "Mitochondrial Quality Control in Age-Related Pulmonary Fibrosis." International Journal of Molecular Sciences 21, no. 2 (January 18, 2020): 643. http://dx.doi.org/10.3390/ijms21020643.

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Idiopathic pulmonary fibrosis (IPF) is age-related interstitial lung disease of unknown etiology. About 100,000 people in the U.S have IPF, with a 3-year median life expectancy post-diagnosis. The development of an effective treatment for pulmonary fibrosis will require an improved understanding of its molecular pathogenesis and the “normal” and “pathological’ hallmarks of the aging lung. An important characteristic of the aging organism is its lowered capacity to adapt quickly to, and counteract, disturbances. While it is likely that DNA damage, chronic endoplasmic reticulum (ER) stress, and accumulation of heat shock proteins are capable of initiating tissue repair, recent studies point to a pathogenic role for mitochondrial dysfunction in the development of pulmonary fibrosis. These studies suggest that damage to the mitochondria induces fibrotic remodeling through a variety of mechanisms including the activation of apoptotic and inflammatory pathways. Mitochondrial quality control (MQC) has been demonstrated to play an important role in the maintenance of mitochondrial homeostasis. Different factors can induce MQC, including mitochondrial DNA damage, proteostasis dysfunction, and mitochondrial protein translational inhibition. MQC constitutes a complex signaling response that affects mitochondrial biogenesis, mitophagy, fusion/fission and the mitochondrial unfolded protein response (UPRmt) that, together, can produce new mitochondria, degrade the components of the oxidative complex or clearance the entire organelle. In pulmonary fibrosis, defects in mitophagy and mitochondrial biogenesis have been implicated in both cellular apoptosis and senescence during tissue repair. MQC has also been found to have a role in the regulation of other protein activity, inflammatory mediators, latent growth factors, and anti-fibrotic growth factors. In this review, we delineated the role of MQC in the pathogenesis of age-related pulmonary fibrosis.

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Costa, José, Patrícia C. Braga, Irene Rebelo, Pedro F. Oliveira, and Marco G. Alves. "Mitochondria Quality Control and Male Fertility." Biology 12, no. 6 (June 6, 2023): 827. http://dx.doi.org/10.3390/biology12060827.

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Mitochondria are pivotal to cellular homeostasis, performing vital functions such as bioenergetics, biosynthesis, and cell signalling. Proper maintenance of these processes is crucial to prevent disease development and ensure optimal cell function. Mitochondrial dynamics, including fission, fusion, biogenesis, mitophagy, and apoptosis, maintain mitochondrial quality control, which is essential for overall cell health. In male reproduction, mitochondria play a pivotal role in germ cell development and any defects in mitochondrial quality can have serious consequences on male fertility. Reactive oxygen species (ROS) also play a crucial role in sperm capacitation, but excessive ROS levels can trigger oxidative damage. Any imbalance between ROS and sperm quality control, caused by non-communicable diseases or environmental factors, can lead to an increase in oxidative stress, cell damage, and apoptosis, which in turn affect sperm concentration, quality, and motility. Therefore, assessing mitochondrial functionality and quality control is essential to gain valuable insights into male infertility. In sum, proper mitochondrial functionality is essential for overall health, and particularly important for male fertility. The assessment of mitochondrial functionality and quality control can provide crucial information for the study and management of male infertility and may lead to the development of new strategies for its management.

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Song, Yu, Saideng Lu, Wen Geng, Xiaobo Feng, Rongjin Luo, Gaocai Li, and Cao Yang. "Mitochondrial quality control in intervertebral disc degeneration." Experimental & Molecular Medicine 53, no. 7 (July 2021): 1124–33. http://dx.doi.org/10.1038/s12276-021-00650-7.

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AbstractIntervertebral disc degeneration (IDD) is a common and early-onset pathogenesis in the human lifespan that can increase the risk of low back pain. More clarification of the molecular mechanisms associated with the onset and progression of IDD is likely to help establish novel preventive and therapeutic strategies. Recently, mitochondria have been increasingly recognized as participants in regulating glycolytic metabolism, which has historically been regarded as the main metabolic pathway in intervertebral discs due to their avascular properties. Indeed, mitochondrial structural and functional disruption has been observed in degenerated nucleus pulposus (NP) cells and intervertebral discs. Multilevel and well-orchestrated strategies, namely, mitochondrial quality control (MQC), are involved in the maintenance of mitochondrial integrity, mitochondrial proteostasis, the mitochondrial antioxidant system, mitochondrial dynamics, mitophagy, and mitochondrial biogenesis. Here, we address the key evidence and current knowledge of the role of mitochondrial function in the IDD process and consider how MQC strategies contribute to the protective and detrimental properties of mitochondria in NP cell function. The relevant potential therapeutic treatments targeting MQC for IDD intervention are also summarized. Further clarification of the functional and synergistic mechanisms among MQC mechanisms may provide useful clues for use in developing novel IDD treatments.

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Mohanraj, Karthik, Urszula Nowicka, and Agnieszka Chacinska. "Mitochondrial control of cellular protein homeostasis." Biochemical Journal 477, no. 16 (August 26, 2020): 3033–54. http://dx.doi.org/10.1042/bcj20190654.

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Mitochondria are involved in several vital functions of the eukaryotic cell. The majority of mitochondrial proteins are coded by nuclear DNA. Constant import of proteins from the cytosol is a prerequisite for the efficient functioning of the organelle. The protein import into mitochondria is mediated by diverse import pathways and is continuously under watch by quality control systems. However, it is often challenged by both internal and external factors, such as oxidative stress or energy shortage. The impaired protein import and biogenesis leads to the accumulation of mitochondrial precursor proteins in the cytosol and activates several stress response pathways. These defense mechanisms engage a network of processes involving transcription, translation, and protein clearance to restore cellular protein homeostasis. In this review, we provide a comprehensive analysis of various factors and processes contributing to mitochondrial stress caused by protein biogenesis failure and summarize the recovery mechanisms employed by the cell.

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Dissertations / Theses on the topic "Mitochondrial biogenesis and quality control"

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Jong, Liesbeth de. "Regulated assembly of the respiratory chain in Saccharomyces cerevisiae involvement of the mitochondrial NAD-linked isocitrate dehydrogenase, (AAA-)metallo-proteases and prohibitin in synthesis, quality control, turnover and stability /." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/87355.

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Leung, Eileen. "Quality control in the biogenesis of the signal recognition particle." Thesis, University of Newcastle upon Tyne, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506530.

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Ostojic, Jelena. "Control of the biogenesis of the OXPHOS complexes and their interactions in Saccharomyces cerevisiae." Thesis, Evry-Val d'Essonne, 2013. http://www.theses.fr/2013EVRY0013/document.

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Le complexe III de la chaine respiratoire mitochondriale (OXPHOS III) chez S. cerevisiae est assemblé à partir de dix sous-unités structurales codées par le génome soit nucléaire, soit mitochondrial et fait intervenir une douzaine de protéines extrinsèques au complexe. Nous avons étudié l’une d’entre elle, Bcs1, une ATPase oligomérique conservée de la famille des protéines AAA (ATPases Associated with diverse cellular Activities), qui contrôle la dernière étape de l’assemblage du complexe III. Chez l’Homme, des mutations dans l’orthologue de BCS1, BCS1L, sont associées à différentes maladies. Nous avons montré que des mutations dans les résidus conservés du domaine AAA de Bcs1 peuvent être compensées par des mutations dans les sous-unités de l’ATP synthase mitochondriale (OXPHOS V). Ces mutations compensatrices diminuent toutes l’activité d’hydrolyse de l’ATP de l’enzyme et nous avons proposé que la biogenèse du complexe III puisse être modulée selon l’état énergétique mitochondrial par Bcs1 via sa dépendance à l’ATP. Nous avons aussi identifié des mutations compensatrices dans d’autres gènes et le cas particulier de la délétion du RRF1, facteur général du recyclage des ribosomes mitochondriaux, a été étudié. Nous avons montré que l’absence de Rrf1 a un effet différent sur la stabilité et la traduction des divers ARNm mitochondriaux. Nos résultats suggèrent une coopération entre les facteurs généraux et les facteurs spécifiques de la traduction mitochondriale dans le contrôle de l’expression des sous-unités des complexes OXPHOS traduites dans la mitochondrie
OXPHOS complexes are multi-subunit complexes embedded in the inner mitochondrial membrane. We have studied the assembly factor Bcs1 that is a membrane-bound AAA-ATPase, required for the assembly of complex III. Mutations in the human gene BCS1L are responsible for various mild to lethal pathologies. Extragenic compensatory mutations able to restore the assembly of complex III in yeast bcs1 mutants were found in different genes not directly connected to the complex, revealing new networks of protein interactions. Mutations in catalytic subunits of ATP synthase were identified and thoroughly characterized. This work has allowed us to propose a novel regulatory loop via the ATP-dependent activity of Bcs1 protein, connecting the production of mitochondrial complex III and the activity of the ATP synthase. Moreover, these results hold promise for the development of therapies, targeting the mitochondrial adenine nucleotide pool, in treatment of BCS1-based disorders. We also show that the absence of RRF1, a mitochondrial ribosome recycling factor, is able to compensate defects of bcs1 mutants. Deletion of RRF1 has a differential impact on the stability and translation of mitochondrial mRNAs. Our results suggest cooperation between general and specific translation factors in controlling the expression of mtDNA-encoded subunits of the OXPHOS complexes

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MacVicar, Thomas D. B. "Autophagy and mitochondrial quality control in homeostasis and disease." Thesis, University of Bristol, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627943.

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Mitochondria are the powerhouses of eukaryotic cells and they must remain healthy in order to generate sufficient ATP for cellular function. Dysfunctional mitochondria pose a grave threat to high-energy demanding tissues and are associated with an array of human diseases. Mitochondria exist in a dynamic organelle network that is essential for their intracellular distribution and quality control. A damaged mitochondrion must first be exiled from the network by mitochondrial fission and next be neutralized by a process termed mitophagy. A number of mitophagy pathways exist to specifically target damaged or redundant mitochondria for engulfment by double-membrane autophagosomes in order to deliver them to the acidic lysosome for degradation. This dissertation explores the regulation and molecular mechanisms of the PINK1/Parkin mitophagy pathway. Mutated in several forms of Parkinson's disease, the PINK1 kinase and Parkin E3-ubiquitin ligase govern the selective degradation of dysfunctional mitochondria and they have been demonstrated to play key neuroprotective roles in vitro and in vivo. Here, the role of mitochondrial bioenergetics in regulating mitophagy is investigated. By employing a range of biochemical and imaging techniques in a cell-based model of Parkin-mediated mitophagy, the following data demonstrate how cells dependent on mitochondrial respiration can avoid mitophagy via intricate control of mitochondrial dynamics. In order to maintain the energy supply, respiring cells can resist mitophagy by preserving an interconnected mitochondrial network via inhibition of Drp1 and impaired OMA1-dependent OPA1 cleavage. This dissertation also questions the importance of close contact between the mitochondria and endoplasmic reticulum (ER) for the progression of Parkin-mediated mitophagy. A focused siRNA screen of ER-mitochondrial communication factors highlights a novel role for ER-mitochondrial Ca2+ signa ling during Parkin-mediated mitophagy. Together, the data presented in this dissertation place mitochondrial bioenergetic demand and Ca2+ flux as key players in the regulation of mitophagy. Further research will be required to identify whether these two regulatory arms are linked and will strengthen the therapeutic potential for positively modulating mitochondrial homeostasis in order to promote cell protection.

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Ling, Jiqiang. "Role of phenylalanyl-tRNA synthetase in translation quality control." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1212111223.

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Vigié, Pierre. "Mitochondrial quality control : roles of autophagy, mitophagy and the proteasome." Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0202/document.

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La mitophagie, la dégradation sélective des mitochondries par autophagie, est impliquée dans l’élimination des mitochondries endommagées ou superflues et requiert des régulateurs et protéines spécifiques. Chez la levure, Atg32, localisée dans la membrane externe mitochondriale, interagit avec Atg8, et permet le recrutement des mitochondries et leur séquestration à l’intérieur des autophagosomes. Atg8 est conjuguée à de la phosphatidyléthanolamine et est ainsi ancrée aux membranes du phagophore et des autophagosomes. Chez la levure, plusieurs voies de synthèse de PE existent mais leur contribution dans l’autophagie et la mitophagie est inconnue. Dans le premier chapitre, nous avons étudié la contribution des différentes enzymes de synthèse de PE, dans l’induction de l’autophagie et la mitophagie et nous avons démontré que Psd1, la phosphatidylsérine décarboxylase mitochondriale, est impliquée dans la mitophagie seulement en condition de carence azotée alors que Psd2, localisée dans les membranes vacuolaires, endosomales et de l’appareil de Golgi, est nécessaire en phase stationnaire de croissance. Dans le second chapitre, la relation entre Atg32, la mitophagie et le protéasome a été étudiée. Nous avons démontré que l’activité du promoteur d’ATG32 et la quantité de protéine Atg32 exprimée sont inversement régulées. En phase stationnaire de croissance, l’inhibition du protéasome empêche la diminution de l’expression d’Atg32 et la mitophagie est stimulée. Nos données montrent ainsi que la quantité d’Atg32 est reliée à l’activité du protéasome et que cette protéine pourrait être ubiquitinylée. Dans le troisième chapitre, nous nous sommes intéressés au rôle potentiel de Dep1, un composant du complexe nucléaire Rpd3 d’histones déacétylases, dans la mitophagie. Dans nos conditions, Dep1 semble être mitochondriale et elle est impliquée dans la régulation de la mitophagie. BRMS1L (Breast Cancer Metastasis suppressor 1-like) est l’homologue de Dep1 chez les mammifères. Cette protéine possède un rôle anti-métastatique dans des lignées de cancer du sein. Nous avons trouvé que l’expression de BRMS1L augmente en présence de stimuli pro-mitophagie
Mitophagy, the selective degradation of mitochondria by autophagy, is implicated in the clearance of superfluous or damaged mitochondria and requires specific proteins and regulators. In yeast, Atg32, an outer mitochondrial membrane protein, interacts with Atg8, promoting mitochondria recruitment to the phagophore and their sequestration within autophagosomes. Atg8 is anchored to the phagophore and autophagosome membranes thanks to phosphatidylethanolamine (PE). In yeast, several PE synthesis pathways have been characterized, but their contribution to autophagy and mitophagy is unknown. In the first chapter, we investigated the contribution of the different enzymes responsible for PE synthesis in autophagy and mitophagy and we demonstrated that Psd1, the mitochondrial phosphatidylserine decarboxylase, is involved in mitophagy induction only in nitrogen starvation, whereas Psd2, located in vacuole/Golgi apparatus/endosome membranes, is required preferentially for mitophagy induction in stationary phase of growth. In the second chapter, we were interested in the relationship between Atg32, mitophagy and the proteasome. We demonstrated that ATG32 promoter activity and protein expression are inversely regulated. During stationary phase of growth, proteasome inhibition abolishes the decrease in Atg32 expression and mitophagy is enhanced. Our data indicate that Atg32 protein is regulated by the proteasome activity and could be ubiquitinated. In the third chapter, we investigated the involvement of Dep1, a member of the nuclear Rpd3L histone deacetylase complex, in mitophagy. In our conditions, Dep1 seems to be located in mitochondria and is a novel effector of mitophagy both in nitrogen starvation and stationary phase of growth. BRMS1L (Breast Cancer Metastasis suppressor 1-like) is the mammalian homolog of Dep1 and has been described in breast cancer metastasis suppression. We found that BRMS1L protein expression increases upon pro-mitophagy stimuli

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Lingiah, Krishna Anand. "The role of DJ-1 in enhancing mitochondrial quality control." Thesis, Boston University, 2013. https://hdl.handle.net/2144/12148.

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Thesis (M.A.)--Boston University
DJ-1 is a cytosolic sensor for oxidative damage which acts on the Mitochondria. It works to curb the negative effects of high membrane potential in mitochondria, but the mechanism of action is still uncertain. This study measured DJ-1’s potential in enchancing mitochondrial quality control in the context of pancreatic B-cells treated with a palmitate and glucose media to promote glucolipotoxicity (GLT). DJ-1 was proven capable of reversing GLT induced changed in mitochondrial morphology in the arenas of Feret’s diameter, aspect ratio, and form factor. We also showed that the mitochondrial membrane potential did not vary with the presence or absence of DJ-1. In addition, DJ-1 was shown capable of limiting the upward boundary of GLT induced increase in mitochondrial membrane potential. Furthermore, an experiment using INS1 cells with GFP-LC3 showed that DJ-1 can decrease the average number of autophagosomes in the cell.

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Ng, Cheuk-Him (Andy). "Genome-Wide Screen Identifies Novel Genes Involved in Mitochondrial Quality Control." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/33204.

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In addition to ATP generation, mitochondria are essential in various cellular processes ranging from biosynthetic pathways, apoptosis, cell cycle progression, and calcium buffering. Studies in living cells have now firmly established that mitochondria exist as a dynamic network sculpted by fission and fusion reactions, rather than separated, individual organelles. Not surprisingly, mutations in genes involved in mitochondrial dynamics and quality control lead to human diseases such as Charcot-Marie-Tooth disease type 2A, Optic atrophy, and autosomal recessive Parkinson disease. I have designed a high-throughput protocol to permit genome-wide screening for novel genes that are required for normal mitochondrial morphology. I have executed a genome-wide RNA interference screen and identified several novel genes required for mitochondrial dynamics in addition to known regulators of mitochondrial dynamics. A detailed high-throughput genome-wide screening protocol is presented. I have shown that TID1, a gene identified from the screen, has a dual-role in maintaining the integrity of mitochondrial DNA and preventing the aggregation of complex I subunits. My analysis of the mitochondrial role of TID1 supports the existence of a TID1- mediated stress response to ATP synthase inhibition. The genome screen also identified the novel gene ROMO1 as essential for normal mitochondrial morphology. I have shown that ROMO1 may have an additional role in maintaining mitochondrial spare respiratory capacity, possibly by affecting cellular substrate availability. Finally, in a collaborative effort, we have shown that homozygous mutations in the mitochondrial fusion gene MFN2 lead to multiple symmetric lipomatosis (MSL) associated with neuropathy. Mechanistically, this mutation reduces MFN2 homocomplex formation. Taken together, these results show the utility of genome-wide screening in identifying genes involved in mitochondrial quality control.

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Rüb, Cornelia [Verfasser]. "The Parkinson’s disease-related kinase Pink1 mediates mitochondrial quality control / Cornelia Rüb." Bonn : Universitäts- und Landesbibliothek Bonn, 2016. http://d-nb.info/1119888662/34.

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Eira, da Costa Ana Carina. "Analysis of mitochondrial quality control using a Drosophila model of Parkinson's disease." Thesis, University of Leicester, 2013. http://hdl.handle.net/2381/28019.

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Parkinson’s disease (PD) is the most common neurodegenerative movement disorder. Despite recent advances, the cause for most PD cases remains unclear. The discovery of mutations in PINK1 (PTEN-induced putative kinase 1) reinforced the importance of mitochondrial impairment in PD. Mitochondria are essential organelles for energy generation in eukaryotic cells, whose compromise can eventually cause cell death. Multicellular organisms have evolved quality control mechanisms to ensure the viability of mitochondria and ultimately the cell. Molecular quality control through the mitochondrial chaperones and proteases acts to promote the proper folding of polypeptides and the degradation of misfolded or damaged proteins. When molecular quality control is overwhelmed, organellar quality control ensures mitochondrial recycling through a selective form of autophagy called mitophagy. PINK1 has been proposed to act in both molecular and organellar quality control, by modulating the activity of chaperones, namely HtrA2 and TRAP1, and acting on mitophagy through Parkin recruitment to damaged mitochondria. The work in this thesis provides evidence of a genetic interaction between Trap1, Pink1 and parkin in Drosophila melanogaster. Trap1 is essential to maintain mitochondrial and dopaminergic neuronal functions and is associated with resistance to stress. Importantly, neuronal expression of Trap1 is sufficient to rescue the Pink1 mutants. Moreover, the expression of Trap1 ameliorates parkin-mutant phenotypes and parkin expression suppresses Trap1-mutant phenotypes, suggesting that molecular and organellar quality control pathways act in parallel downstream from Pink1. p62 is an autophagy adaptor that acts in the PINK1/Parkin pathway, facilitating the aggregation and elimination of depolarised mitochondria through mitophagy. In this work it is shown that loss-of-function mutations in the Drosophila orthologue of p62, ref(2)P, result in a reduction in lifespan and age-dependent neurodegeneration. ref(2)P expression rescues the Pink1-mutant phenotypes and its presence is essential for the parkin-mediated rescue of Pink1 mutant flies.

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Books on the topic "Mitochondrial biogenesis and quality control"

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Zhou, Hao, Rui Guo, Amanda Lochner, Russel J. Reiter, and Hsueh-Hsiao Wang, eds. Role of Mitochondrial Quality Control in Myocardial and Microvascular Physiology and Pathophysiology. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-547-3.

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Book chapters on the topic "Mitochondrial biogenesis and quality control"

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Mears, Jason A. "Mitochondrial Biogenesis and Quality Control." In The Structural Basis of Biological Energy Generation, 451–76. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-8742-0_24.

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Bross, Peter, Elena I. Rugarli, Giorgio Casari, and Thomas Langer. "Protein quality control in mitochondria and neurodegeneration in hereditary spastic paraplegia." In Mitochondrial Function and Biogenesis, 97–121. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/b95865.

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Luzikov, Valentin N., and Donald B. Roodyn. "Control Over Mitochondrial Assembly." In Mitochondrial Biogenesis and Breakdown, 256–88. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-1650-3_8.

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Vega, Rick B., Teresa C. Leone, and Daniel P. Kelly. "Transcriptional Control of Mitochondrial Biogenesis and Maturation." In Cardiac Energy Metabolism in Health and Disease, 89–102. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1227-8_6.

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Hood, David A., Beatrice Chabi, Keir Menzies, Michael O’Leary, and Donald Walkinshaw. "Exercise-Induced Mitochondrial Biogenesis in Skeletal Muscle." In Role of Physical Exercise in Preventing Disease and Improving the Quality of Life, 37–60. Milano: Springer Milan, 2007. http://dx.doi.org/10.1007/978-88-470-0376-7_3.

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Wang, Rui, and Guanghui Wang. "Autophagy in Mitochondrial Quality Control." In Autophagy: Biology and Diseases, 421–34. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0602-4_19.

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Eskins, K. "Light Quality and Irradiance Level Interaction in Control of Chloroplast Development." In Regulation of Chloroplast Biogenesis, 505–9. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3366-5_73.

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Luce, Karin, Andrea C. Weil, and Heinz D. Osiewacz. "Mitochondrial Protein Quality Control Systems in Aging and Disease." In Advances in Experimental Medicine and Biology, 108–25. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7002-2_9.

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Voos, Wolfgang, Linda A. Ward, and Kaye N. Truscott. "The Role of AAA+ Proteases in Mitochondrial Protein Biogenesis, Homeostasis and Activity Control." In Subcellular Biochemistry, 223–63. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-5940-4_9.

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de Boer, Lonneke, Maaike C. de Vries, Jan A. M. Smeitink, and Werner J. H. Koopman. "Disorders of Mitochondrial Homeostasis, Dynamics, Protein Import, and Quality Control." In Physician's Guide to the Diagnosis, Treatment, and Follow-Up of Inherited Metabolic Diseases, 889–913. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-67727-5_46.

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Conference papers on the topic "Mitochondrial biogenesis and quality control"

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Kraft, B. D., H. B. Suliman, E. N. Pavlisko, V. L. Roggli, and C. A. Piantadosi. "Alveolar Mitochondrial Quality Control During Acute Respiratory Distress Syndrome." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5591.

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Шунькина, Дарья Александровна, Александра Андреевна Комар, Мария Александровна Вульф, Елена Витальевна Кириенкова, and Лариса Сергеевна Литвинова. "PLASMA IL-6 IS ASSOCIATED WITH DECREASED TFAM GENE EXPRESSION IN THE LIVER IN OBESE PATIENTS WITH TYPE 2 DIABETES." In Фундаментальные и прикладные исследования. Актуальные проблемы и достижения: сборник избранных статей Всероссийской (национальной) научной конференции (Санкт-Петербург, Декабрь 2021). Crossref, 2022. http://dx.doi.org/10.37539/fipi323.2021.56.58.002.

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Биогенез митохондрий регулируется организованной индукции нескольких транскрипционных факторов. Утрата митохондриальной адаптации способствует сахарному диабету 2 типа. Высокий уровень IL-6 в плазме крови пациентов с ожирением взаимосвязан со снижением экспрессии гена TFAM в биоптатах печени. Уровень экспрессии гена TFAM в биоптатах печени у больных с СД 2 типа снижался относительно контрольной группы. Mitochondrial biogenesis is regulated by the organized induction of several transcription factors. Loss of mitochondrial adaptation contributes to type 2 diabetes. A high level of IL-6 in the blood plasma of obese patients is associated with a decrease in TFAM gene expression in liver biopsies. The expression level of the TFAM gene in liver biopsies of patients with type 2 diabetes decreased relative to the control group.

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Jeyaraju, Danny V., Veronique Voisin, Ashwin Ramakrishnan, Rose Hurren, Neil Maclean, Marcela Gronda, Mark Minden, Gary Bader, and Aaron D. Schimmer. "Abstract A87: Targeting the mitochondrial quality control machinery in acute myeloid leukemia." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-a87.

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Kamino, Hiroki, Yasuyuki Nakamura, Noriaki Kitamura, Manabu Futamura, Masaki Yoshida, Ryuya Murai, Yuri Saito, et al. "Abstract 1687: Frequent inactivation of the Mieap-regulated mitochondrial quality control in colorectal cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1687.

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Kamino, Hiroki, Yasuyuki Nakamura, Hitoya Sano, Ryuya Murai, Yuri Saito, Manabu Futamura, Kazuhiro Yoshida, et al. "Abstract 320: Frequent inactivation of the Mieap-regulated mitochondrial quality control in pancreatic and breast cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-320.

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Tohme, Samer, Hamza Yazdani, Richard L. Simmons, Allan Tsung, and David Bartlett. "Abstract 2818: Neutrophil extracellular traps regulate mitochondrial quality control in cancer cells to promote tumor growth." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2818.

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Tohme, Samer, Hamza Yazdani, Richard L. Simmons, Allan Tsung, and David Bartlett. "Abstract 2818: Neutrophil extracellular traps regulate mitochondrial quality control in cancer cells to promote tumor growth." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2818.

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Sano, Hitoya, Hiroki Kamino, Yasuyuki Nakamura, Masaki Yoshida, Ryuya Murai, Yuri Saito, Manabu Futamura, Kazuhiro Yoshida, and Hirofumi Arakawa. "Abstract LB-132: Frequent inactivation of the p53/Mieap/BNIP3 mitochondrial quality control pathway in gastric cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-lb-132.

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Futamura, Manabu, Hitoya Sano, Siqin Gaowa, Akira Nakakami, Kazuhiro Yoshida, and Hirofumi Arakawa. "Abstract 4786: Potential role of p53-Mieap-regulated mitochondrial quality control as a tumor suppressor in gastric and esophageal cancers Potential role of p53/Mieap-regulated mitochondrial quality control as a tumor suppressor in gastric, esophageal and breast cancers." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4786.

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Futamura, M., S. Gaowa, H. Arakawa, and K. Yoshida. "Abstract P3-09-04: Possible role of p53/Mieap-regulated mitochondrial quality control as a tumor suppressor in human breast cancer." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p3-09-04.

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Reports on the topic "Mitochondrial biogenesis and quality control"

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Chen, Junping, Zach Adam, and Arie Admon. The Role of FtsH11 Protease in Chloroplast Biogenesis and Maintenance at Elevated Temperatures in Model and Crop Plants. United States Department of Agriculture, May 2013. http://dx.doi.org/10.32747/2013.7699845.bard.

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specific objectives of this proposal were to: 1) determine the location, topology, and oligomerization of FtsH11 protease; 2) identify the substrate/s of FtsH11 and the downstream components involved in maintaining thermostability of chloroplasts; 3) identify new elements involved in FtsH11 protease regulatory network related to HT adaptation processes in chloroplast; 4) Study the role of FtsH11 homologs from crop species in HT tolerance. Background to the topic: HT-tolerant varieties that maintain high photosynthetic efficiency at HT, and cope better with daily and seasonal temperature fluctuations are in great need to alleviate the effect of global warming on food production. Photosynthesis is a very complex process requiring accurate coordination of many complex systems and constant adjustments to the changing environments. Proteolytic activities mediated by various proteases in chloroplast are essential part of this process and critical for maintaining normal chloroplast functions under HT. However, little is known about mechanisms that contribute to adaptation of photosynthetic processes to HT. Our study has shown that a chloroplast-targeted Arabidopsis FtsH11 protease plays an essential and specific role in maintaining thermostability of thylakoids and normal photosynthesis at moderate HT. We hypothesized that FtsH11 homologs recently identified in other plant species might have roles similarly to that of AtFtsH1. Thus, dissecting the underlying mechanisms of FtsH11 in the adaptation mechanisms in chloroplasts to HT stress and other elements involved will aid our effort to produce more agricultural products in less favorable environments. Major conclusions, solutions, achievements - Identified the chloroplast inner envelope membrane localization of FtsH11. - Revealed a specific association of FtsH11 with the a and b subunits of CPN60. - Identified the involvement of ARC6, a protein coordinates chloroplast division machineries in plants, in FtsH11 mediated HT adaptation process in chloroplast. -Reveal possible association of a polyribonucleotide nucleotidyltransferase (cpPNPase), coded by At3G03710, with FtsH11 mediated HT adaptation process in chloroplast. - Mapped 4 additional loci in FtsH11 mediated HT adaptation network in chloroplast. - Demonstrated importance of the proteolytic activity of FtsH11 for thermotolerance, in addition to the ATPase activity. - Demonstrated a conserved role of plant FtsH11 proteases in chloroplast biogenesis and in maintaining structural and functional thermostability of chloroplast at elevated temperatures. Implications, both scientific and agricultural:Three different components interacting with FtsH11 were identified during the course of this study. At present, it is not known whether these proteins are directly involved in FtsH11mediated thermotolerance network in chloroplast and/or how these elements are interrelated. Studies aiming to connect the dot among biological functions of these networks are underway in both labs. Nevertheless, in bacteria where it was first studied, FtsH functions in heat shock response by regulating transcription level of σ32, a heat chock factor regulates HSPsexpression. FtsH also involves in control of biosynthesis of membrane components and quality control of membrane proteins etc. In plants, both Arc 6 and CPN60 identified in this study are essential in chloroplast division and developments as mutation of either one impairs chloroplast division in Arabidopsis. The facts that we have found the specific association of both α and β CPN60 with FtsH11 protein biochemically, the suppression/ enhancement of ftsh11 thermosensitive phenotype by arc6 /pnp allele genetically, implicate inter-connection of these networks via FtsH11 mediated network(s) in regulating the dynamic adaptation processes of chloroplast to temperature increases at transcriptional, translational and post-translational levels. The conserved role of FtsH11 proteases in maintaining thermostability of chloroplast at HT demonstrated here provides a foundation for improving crop photosynthetic performance at high temperatures.

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Blumwald, Eduardo, and Avi Sadka. Citric acid metabolism and mobilization in citrus fruit. United States Department of Agriculture, October 2007. http://dx.doi.org/10.32747/2007.7587732.bard.

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Accumulation of citric acid is a major determinant of maturity and fruit quality in citrus. Many citrus varieties accumulate citric acid in concentrations that exceed market desires, reducing grower income and consumer satisfaction. Citrate is accumulated in the vacuole of the juice sac cell, a process that requires both metabolic changes and transport across cellular membranes, in particular, the mitochondrial and the vacuolar (tonoplast) membranes. Although the accumulation of citrate in the vacuoles of juice cells has been clearly demonstrated, the mechanisms for vacuolar citrate homeostasis and the components controlling citrate metabolism and transport are still unknown. Previous results in the PIs’ laboratories have indicated that the expression of a large number of a large number of proteins is enhanced during fruit development, and that the regulation of sugar and acid content in fruits is correlated with the differential expression of a large number of proteins that could play significant roles in fruit acid accumulation and/or regulation of acid content. The objectives of this proposal are: i) the characterization of transporters that mediate the transport of citrate and determine their role in uptake/retrieval in juice sac cells; ii) the study of citric acid metabolism, in particular the effect of arsenical compounds affecting citric acid levels and mobilization; and iii) the development of a citrus fruit proteomics platform to identify and characterize key processes associated with fruit development in general and sugar and acid accumulation in particular. The understanding of the cellular processes that determine the citrate content in citrus fruits will contribute to the development of tools aimed at the enhancement of citrus fruit quality. Our efforts resulted in the identification, cloning and characterization of CsCit1 (Citrus sinensis citrate transporter 1) from Navel oranges (Citrus sinesins cv Washington). Higher levels of CsCit1 transcripts were detected at later stages of fruit development that coincided with the decrease in the juice cell citrate concentrations (Shimada et al., 2006). Our functional analysis revealed that CsCit1 mediates the vacuolar efflux of citrate and that the CsCit1 operates as an electroneutral 1CitrateH2-/2H+ symporter. Our results supported the notion that it is the low permeable citrateH2 - the anion that establishes the buffer capacity of the fruit and determines its overall acidity. On the other hand, it is the more permeable form, CitrateH2-, which is being exported into the cytosol during maturation and controls the citrate catabolism in the juice cells. Our Mass-Spectrometry-based proteomics efforts (using MALDI-TOF-TOF and LC2- MS-MS) identified a large number of fruit juice sac cell proteins and established comparisons of protein synthesis patterns during fruit development. So far, we have identified over 1,500 fruit specific proteins that play roles in sugar metabolism, citric acid cycle, signaling, transport, processing, etc., and organized these proteins into 84 known biosynthetic pathways (Katz et al. 2007). This data is now being integrated in a public database and will serve as a valuable tool for the scientific community in general and fruit scientists in particular. Using molecular, biochemical and physiological approaches we have identified factors affecting the activity of aconitase, which catalyze the first step of citrate catabolism (Shlizerman et al., 2007). Iron limitation specifically reduced the activity of the cytosolic, but not the mitochondrial, aconitase, increasing the acid level in the fruit. Citramalate (a natural compound in the juice) also inhibits the activity of aconitase, and it plays a major role in acid accumulation during the first half of fruit development. On the other hand, arsenite induced increased levels of aconitase, decreasing fruit acidity. We have initiated studies aimed at the identification of the citramalate biosynthetic pathway and the role(s) of isopropylmalate synthase in this pathway. These studies, especially those involved aconitase inhibition by citramalate, are aimed at the development of tools to control fruit acidity, particularly in those cases where acid level declines below the desired threshold. Our work has significant implications both scientifically and practically and is directly aimed at the improvement of fruit quality through the improvement of existing pre- and post-harvest fruit treatments.

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