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358 results for “Mitochondria”
Reduction of elevated proton leak rejuvenates mitochondria in the aged cardiomyocyte
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Data from: Home loving boreal hare mitochondria survived several invasions in Iberia: the relative roles of recurrent hybridisation and allele surfing
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Data from: Prior reproduction alters how mitochondria respond to an oxidative event
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Mitochondria as environments for the nuclear genome in Drosophila: Mitonuclear GxGxE
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Data from: Sibling rivalry vs mother's curse: can kin competition facilitate a response to selection on male mitochondria?
<p>Assuming that fathers never transmit mitochondrial DNA (mtDNA) to their offspring, mitochondrial mutations that affect male fitness are invisible to direct selection on males, leading to an accumulation of male-harming alleles in the mitochondrial genome (mother's curse). However, male phenotypes encoded by mtDNA can still undergo adaptation via kin selection provided that males interact with females carrying related mtDNA, such as their sisters. Here, using experiments with <i>Drosophila melanogaster</i> carrying standardised nuclear DNA but distinct mitochondrial DNA, we test whether the mitochondrial haplotype carried by interacting pairs of larvae affects survival to adulthood, as well as the fitness of the adults. Although mtDNA had no detectable direct or indirect genetic effect on larva-to-adult survival, the fitness of male and female adults was significantly affected by their own mtDNA and the mtDNA carried by their social partner in the larval stage. Thus, mtDNA mutations that alter the effect of male larvae on nearby female larvae (which often carry the same mutation, due to kinship) could theoretically respond to kin selection. We discuss the implications of our findings for the evolution of mitochondria and other maternally inherited endosymbionts.</p>
Convergent adaptation in mitochondria of phylogenetically distant birds: does it exist?
<p><span>In a wide range of taxa, proteins encoded by mitochondrial genomes are involved in adaptation to lifestyle that requires oxygen starvation or elevation of metabolism rate. It remains poorly understood to what extent adaptation to similar conditions is associated with parallel changes in these proteins. We search for genetic signal of parallel or convergent evolution in recurrent molecular adaptation to high altitude, migration, diving, wintering, unusual flight abilities, or loss of flight in mitochondrial genomes of birds. Developing on previous work, we design an approach for detection of recurrent coincident changes in genotype and phenotype, indicative of an association between the two. We describe a number of candidate sites involved in recurrent adaptation in ND genes. However, we find that the majority of convergence events can be explained by random coincidences without invoking adaptation.</span></p>
Mitochondrial oxygen consumption and reactive oxygen species production in hepatopancreas mitochondria of Mya arenaria acclimated under different oxygen regimes
<p>These are the metadata for a publication "Effects of variable oxygen regimes on mitochondrial bioenergetics and reactive oxygen species production in a marine bivalve <em>Mya arenaria</em>" under consideration for publication in the Journal Of Experimental Biology. To study the impacts of different oxygen regimes, we exposed a common sediment-dwelling bivalve, the soft-shell clam <em>Mya arenaria</em>, for 21 days to chronic hypoxia (P<sub>O2</sub>~4.1 kPa), cyclic hypoxia (P<sub>O2</sub>~12.7-1.9 kPa, mean = 5.7 kPa), or normoxia (P<sub>O2</sub>~21.1 kPa). pH was manipulated to mimic the covariation in CO<sub>2</sub>/pH and oxygen levels in coastal hypoxic zones. Mitochondrial respiration, including the proton leak, the capacity for oxidative phosphorylation (OXPHOS), the maximum activity of the electron transport system (ETS), reactive oxygen species (ROS) production, and activity and oxygen affinity of cytochrome c oxidase (CCO) were assessed. Acclimation to constant hypoxia did not affect the studied mitochondrial traits except for a modest decrease in the OXPHOS coupling efficiency. Cyclic hypoxia had no effect on the OXPHOS or ETS capacity, but increased the proton leak and lowered the mitochondrial OXPHOS coupling efficiency. Furthermore, mitochondria of clams acclimated to cyclic hypoxia had higher rates of ROS generation compared with the clams acclimated to normoxia or chronic hypoxia. CCO activity was upregulated under the cyclic hypoxia, but oxygen affinity of CCO did not change. These findings indicate that long-term cyclic hypoxia has a stronger impact on the mitochondria of <em>M. arenaria</em> than chronic hypoxia and might lead to impaired ATP synthesis, higher costs of the mitochondrial maintenance and oxidative stress. These changes might negatively affect populations of <em>M. arenaria</em> in the coastal Baltic Sea under increasing hypoxia pressure.</p>
Data from: Bounds to parapatric speciation: A dobzhansky-muller incompatibility model involving autosomes, X chromosomes and mitochondria
We investigate the conditions for the origin and maintenance of postzygotic isolation barriers, so called (Bateson-)Dobzhansky-Muller incompatibilities or DMIs, among populations that are connected by gene flow. Specifically, we compare the relative stability of pairwise DMIs among autosomes, X chromosomes, and mitochondrial genes. In an analytical approach based on a continent-island framework, we determine how the maximum permissible migration rates depend on the genomic architecture of the DMI, on sex bias in migration rates, and on sex-dependence of allelic and epistatic effects, such as dosage compensation. Our results show that X-linkage of DMIs can enlarge the migration bounds relative to autosomal DMIs or autosome-mitochondrial DMIs, in particular in the presence of dosage compensation. The effect is further strengthened with male-biased migration. This mechanism might contribute to a higher density of DMIs on the X chromosome (large X-effect) that has been observed in several species clades. Furthermore, our results agree with empirical findings of higher introgression rates of autosomal compared to X-linked loci.
Structural conversion of α-synuclein at the mitochondria induces neuronal toxicity; Data sets
<p>Lists of data sets included in <strong>"Structural conversion of α-synuclein at the mitochondria induces neuronal toxicity"</strong></p> <p> </p> <p>Single-molecule confocal Quantification_Images (SNCA-A53T TIRF Images)</p> <p>TIRF Image Quantification</p> <p>TIRF Emission Data</p> <p>Single Vesicle Emission Data</p> <p>DLS Emission Data</p> <p>CD Measurements</p> <p>Amyloid Fibril TIRFM Emission Data </p> <p>α-Syn WT, A53T, A30P and E46K Confirmatory LCMS </p> <p>SNCA A53T iPSC mutation confirmatory Sanger Sequencing</p> <p>ELISA</p> <p>Immunocytochemistry (MAP2 and TRB1)</p> <p>Pierce BCA Protein Assay</p> <p>Aggregation Assay</p> <p>Copy of Empiar_upload_info (CLEM quantification); metadata spreadsheet for TEM and FIB-SEM Image Quantification</p> <p>Live-cell imaging data</p> <ul> <li>Superoxide Emission Data</li> <li>MitoTracker® Red Emission Data</li> <li>MembranePotentialEmissionData (the same experiment for ' TMRM Emission data')</li> <li>Ca 2+ Emission Data</li> <li>NADH Autofluorescence and Redox Quantification</li> <li>ATP Emission Data</li> <li>mPTP Emission Data</li> <li>Cell Death Emission Data (PI & SYTOX)</li> <li>FRET Emission Data</li> <li>MitoTracker® Red Assay</li> <li>Cell Death Assay</li> </ul>
BRD4-mediated epigenetic regulation of endoplasmic reticulum-mitochondria contact sites is governed by the mitochondrial complex III
<p>This is a high content drug screening dataset composed of images and single-cell analysis results from a 384-well plate </p> <p>The SPLICS reporter is composed of a split GFP1-10 barrel localized to the mitochondrial outer membrane, a P2A self-cleavage signal for equimolar expression, and the remaining beta11 fragment targeted to the ER membrane. Upon ERMCS formation within the 8-10 nm distance, the split-GFP reporter forms intact GFP. Doxycycline-inducible SPLICS reporter stable cell lines were generated via a three-plasmid PiggyBac transposase system. Cells were co-transfected with the plasmids using Lipofectamine 2000 transfection reagent, then the next day selected with 2 mg/ml of G418 (Geneticin) for 7 days. With the SPLICS integrated cells, mitochondrial TagRFP is expressed in them. For mitochondrial TagRFP labeling in cells, we utilized a lentiviral backbone and introduced a mitochondria matrix TagRFP (mitoTagRFP) to control for gene expression and monitor mitochondrial abundance. After mitoTagRFP integration, 100 ng/ml of doxycycline were used to induce SPLICS reporter expression, and GFP/TagRFP double positive cells were sorted on Bigfoot Spectral Cell Sorter (Invitrogen) to isolate GFP/TagRFP positive clones. Clones were cultured and screened for accurate localization of SPLICS reporter to mitochondria and ER via live cell imaging and for normal mitochondrial oxygen consumption rate. Probe induction did not have a deleterious effect on cell number or increasing green fluorescence for at least 72 hours of reporter induction. For ERMCS analysis with SPLICS, cells will be induced with 100 ng/ml of doxycycline for minimally 24 hr before treatment or analysis.</p>
Thirdhand smoke induces metabolic alterations associated with mitochondria dysfunction in kidney of exposed mice
<p>This dataset contains all raw LC-MS data of kidney extracts from mice exposed to thirdhand smoke (THS) used in the paper <em>Thirdhand smoke induces metabolic alterations associated with mitochondria dysfunction in kidney of exposed mice</em>.</p> <p><strong>Objective:</strong> The goal of this study is to characterize the THS-induced molecular alterations in kidney using an LC-based untargeted metabolomic approach.</p> <p><strong>Experimental groups</strong>: Kidney extracts were from three mice groups: control group (CTRL, n=3), which was never exposed to THS; THS exposed group (THS, n=5), was exposed to THS from weaning (three weeks of age) to 24 weeks, and THS exposed group under an antioxidant treatment (THS-AO, n=5) was exposed to THS and treated with antioxidants (N-acetylcysteine and α-tocopherol) daily from weaning until the end of the experiment.</p> <p><strong>Sample extraction:</strong> Metabolites were extracted from kidneys using a biphasic mixture of organic solvents containing acetonitrile, Milli-Q water, dichloromethane and methanol. Quality control samples (QCs) were prepared by pooling equal volumes of each extract and analysed every five samples to ensure data quality and reproducibility.</p> <p><strong>LC-MS analysis:</strong> Kidney samples were analysed using a 1290 UHPLC system coupled to a 6550 quadrupole time of flight (QTOF) from Agilent Technologies in ESI+ mode. Chromatographic separation was conducted on a ACQUITY UHPLC BEH HILIC column (1.7 µm, 150 × 2.1 mm, Waters) for aqueous extracts and a an Kinetex EVO C<sub>18</sub> column (1.7 µm, 150 × 2.1 mm, Phenomenex) for lipid extracts.</p> <p><strong>LC-MS files are named following this code:</strong></p> <ol> <li>Extracts: AQ: Aqueous extracts; LIP: Lipid extracts</li> <li>Samples: CTRL: control group; THS: THS exposed group; THS-AO: THS exposed group under an antioxidant treatment.</li> <li>Files: mzDATA: LC-MS raw data in mzXML format; MSMS: MS/MS data used for identification of metabolites in mzXML format.</li> </ol> <p><strong>Technical information</strong></p> <ol> <li>Sample extraction and data acquisition (single date, range, approximate date): 2018-07 to 2018-10</li> <li>Data analysis (single date, range, approximate date): 2019-01 to 2021-06</li> <li>Geographic location of data collection: <ul> <li>Mice exposure: Department of Molecular, Cell and Systems Biology, University of California, Riverside CA 92521, U.S.A</li> <li>Sample extraction and data acquisition: Universitat Rovira i Virgili, Departament d’Enginyeria Electrònica, Elèctrica i Automàtica, Tarragona, Spain.</li> </ul> </li> <li>Information about funding sources that supported the collection of the data: This research was funded by the European Union’s Horizon 2020 research and innovation pro-gramme under the Marie Sklodowska-Curie grant agreement No. 660034; the Secretaria d’Universitats i Recerca del Departament d’Empresa i Coneixement de la Generalitat de Catalunya through C.M.’s predoctoral grant number 2020 FI_B2 00118; the Spanish Ministry of Science & Innovation through N.R.’s Juan de la Cierva Incorporación grant No. (IJCI- 2015-23158); N.R.’s Miguel Servet contract (CP19/00060) from Instituto de Salud Carlos III, co-financed by Fondo Europeo de Desarrollo Regional (FEDER), Unión Europea, “Una manera de hacer Europa”; and the Tobacco-Related Disease Research Program (TRDRP) of the University of California under projects 22RT- 0121 and 23DT-0103.</li> </ol>
Mitochondria
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Clinical Application of Autologous Mitochondria Transplantation for Improving Oocyte Quality.
ClinicalTrials.gov study NCT03639506. IPD Sharing: Not stated. Countries: 0. Publications: 0.
Mitochondria and Chronic Kidney Disease
ClinicalTrials.gov study NCT03177798. IPD Sharing: YES. Countries: 1. Publications: 0.
Convergent adaptation in mitochondria of phylogenetically distant birds: does it exist?
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Data from: Neurotrophins induce fission of mitochondria along embryonic sensory axons
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Data from: Bounds to parapatric speciation: A dobzhansky-muller incompatibility model involving autosomes, X chromosomes and mitochondria
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Data from: Migration, mitochondria, and the yellow-rumped warbler
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Data from: Sibling rivalry vs mother’s curse: can kin competition facilitate a response to selection on male mitochondria?
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IQGAP1 mediates the communication between the nucleus and the mitochondria via NDUFS4 alternative splicing
GEO Series GSE218220. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.