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358 results for “Mitochondria”
Data from: Transplantation of exogenous mitochondria mitigates myocardial dysfunction after cardiac arrest
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Linking performance to powerhouse: Mitochondria functions in blood cells reflect flight endurance of a songbird
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Genotypes and geographic positions of 5797 European white oaks from 636 locations genotyped at 355 nuclear SNPs and 28 maternally inherited SNPs of the chloroplast and mitochondria
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Effects of X-ray irradiation and housing conditions on mitochondria in Peromyscus maniculatus
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Massive RNA editing in ascetosporean mitochondria
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Data from: Functional remodelling of perinuclear mitochondria alters nucleoplasmic Ca2+ signalling in heart failure
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Immuno-engineered mitochondria for efficient therapy of acute organ injuries via modulation of inflammation and cell repair
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Data and code from: Spatial and morphological organization of mitochondria in neurons across a connectome
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Parkin regulates amino acid homeostasis at mitochondria-lysosome (M/L) contact sites in Parkinson’s disease
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Drp1 controls Complex II assembly and skeletal muscle metabolism by Sdhaf2 action on mitochondria
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Glaucoma-associated optineurin mutations increase transcellular degradation of mitochondria in a vertebrate optic nerve
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Data associated with 'Metformin rescues Parkinson's disease phenotypes caused by hyperactive mitochondria'
<p>Metabolic dysfunction occurs in many age-related neurodegenerative diseases, yet its role in disease etiology remains poorly understood. We recently discovered a potential causal link between the branched-chain amino acid transferase, <i>BCAT-1,</i> and the neurodegenerative movement disorder, Parkinson's disease (PD). RNAi-mediated knockdown of <i>C. elegans bcat-1</i> recapitulates PD-like features, including progressive motor deficits and neurodegeneration with age, yet the underlying mechanisms have remained unknown. Using transcriptomic, metabolomic, and imaging approaches, we show here that <i>bcat-1 </i>knockdown increases mitochondrial respiration and induces oxidative damage in neurons through mTOR-independent mechanisms. Increased mitochondrial respiration, or 'mitochondrial hyperactivity,' is required for <i>bcat-1(RNAi)</i> neurotoxicity. Moreover, we show that post-disease onset administration of the type 2 diabetes medication, metformin, reduces mitochondrial respiration to control levels and significantly improves both motor function and neuronal viability. Together, our findings suggest that mitochondrial hyperactivity may be an early event in PD pathogenesis, and strategies aimed at reducing mitochondrial respiration may constitute a surprising new avenue for PD treatment.</p>
Reduction of elevated proton leak rejuvenates mitochondria in the aged cardiomyocyte
<p>Aging-associated diseases, including cardiac dysfunction, are increasingly common in the population. However, the mechanisms of physiologic aging in general, and cardiac aging in particular, remain poorly understood. Age-related heart impairment is lacking a clinically effective treatment. Using the model of naturally aging mice and rats, we show direct evidence of increased proton leak in the aged heart mitochondria. Moreover, our data suggested ANT1 as the most likely site of mediating increased mitochondrial proton permeability in old cardiomyocytes. Most importantly, the tetra-peptide SS-31 prevents age-related excess proton entry, decreases the mitochondrial flash activity and mitochondrial permeability transition pore opening, rejuvenates mitochondrial function by direct association with ANT1 and the mitochondrial ATP synthasome, and leads to substantial reversal of diastolic dysfunction. Our results uncover the excessive proton leak as a novel mechanism of age-related cardiac dysfunction and elucidate how SS-31 is able to reverse this clinically important complication of cardiac aging.</p>
Data from: Mitochondria and Wolbachia titers are positively correlated during maternal transmission
Mothers provide their offspring with symbionts. Maternally transmitted, intracellular symbionts must disperse from mother to offspring with other cytoplasmic elements, like mitochondria. Here, we investigated how the intracellular symbiont Wolbachia interacts with mitochondria during maternal transmission. Mitochondria and Wolbachia may interact antagonistically and compete as each population tries to ensure its own evolutionary success. Alternatively, mitochondria and Wolbachia may cooperate as both benefit from ensuring the fitness of the mother. We characterized the relationship between mitochondria and Wolbachia titers in ovaries of D. melanogaster. We found that mitochondria and Wolbachia titers are positively correlated in common laboratory genotypes of D. melanogaster. We attempted to perturb this covariation through the introduction of Wolbachia variants that colonize at different titers. We also attempted to perturb the covariation through manipulating the female reproductive tract to disrupt maternal transmission. Finally, we also attempted to disrupt the covariation by knocking down gene expression for two loci involved in mitochondrial metabolism: NADH dehydrogenase and a mitochondrial transporter. Overall, we find that mitochondria and Wolbachia titers are commonly positively correlated, but this positive covariation is disrupted at high titers of Wolbachia. Our results suggest that mitochondria and Wolbachia have likely evolved mechanisms to stably coexist, but the competitive dynamics change at high Wolbachia titers. We provide future directions to better understand how their interaction influences the maintenance of the symbiosis.
Data from: Home loving boreal hare mitochondria survived several invasions in Iberia: the relative roles of recurrent hybridisation and allele surfing
Genetic introgression from a resident species into an invading close relative can result from repeated hybridisation along the invasion front and/or allele surfing on the expansion wave. Cases where the phenomenon is massive and systematic, such as for hares (genus Lepus) in Iberia, would be best explained by recurrent hybridisation but this is difficult to prove since the donor populations are generally extinct. In the Pyrenean foothills, Lepus europaeus presumably replaced Lepus granatensis recently and the present species border is parallel to the direction of invasion, so that populations of L. granatensis in the contact zone represent proxies of existing variation before the invasion. Among three pairs of populations sampled across this border, we find less differentiation of mtDNA across than along it, as predicted under recurrent hybridisation at the invasion front. Using autosomal microsatellite loci and X and Y-linked diagnostic loci, we show that admixture across the border is quasi-absent, making it unlikely that lack of interspecific mtDNA differentiation result from ongoing gene flow. Furthermore, we find that the local species ranges are climatically contrasted, making it also unlikely that ongoing ecology-driven movement of the contact account for mtDNA introgression. The lack of mtDNA differentiation across the boundary is mostly due to sharing of mtDNA from a boreal species currently extinct in Iberia (Lepus timidus) whose mitochondria have thus remained in place since the last deglaciation despite successive invasions by two other species. Home loving mitochondria thus witness past species distribution rather than ongoing exchanges across stabilised contact zones.
Figure S3: Immunofluorescence of mitochondria alongside LC3B [FINAL]
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Mitochondria as environments for the nuclear genome in Drosophila: Mitonuclear GxGxE
<p>Mitochondria evolved from a union of microbial cells belonging to distinct lineages that were likely anaerobic. The evolution of eukaryotes required a massive reorganization of the two genomes and eventual adaptation to aerobic environments. The nutrients and oxygen that sustain eukaryotic metabolism today are processed in mitochondria through coordinated expression of 37 mitochondrial genes and over 1000 nuclear genes. This puts mitochondria at the nexus of gene-by-gene (GxG) and gene-by-environment (GxE) interactions that sustain life. Here we use a Drosophila model of mitonuclear genetic interactions to explore the notion that mitochondria are environments for the nuclear genome, and vice versa. We construct factorial combinations of mtDNA and nuclear chromosomes to test for epistatic interactions (GxG), and expose these mitonuclear genotypes to altered dietary environments to examine GxE interactions. We use development time and genome wide RNAseq analyses to assess the relative contributions of mtDNA, nuclear chromosomes, and environmental effects on these traits (mitonuclear GxGxE). We show that the nuclear transcriptional response to alternative mitochondrial 'environments' (GXG) has significant overlap with the transcriptional response of mitonuclear genotypes to altered dietary environments. These analyses point to specific transcription factors (e.g., giant) that mediated these interactions, and identified co-expressed modules of genes that may account for the overlap in differentially expressed genes. Roughly 20% of the transcriptome includes GxG genes that are concordant with GxE genes, suggesting that mitonuclear interactions are part of an organism's environment.</p>
Parthenogenesis doubles the rate of amino acid substitution in Whiptail mitochondria
<p class="MsoNormal"><span>Sexual reproduction is ubiquitous in the natural world, suggesting that sex must have extensive benefits to overcome the cost of males compared to asexual reproduction. One hypothesized advantage of sex with strong theoretical support is that sex plays a role in removing deleterious mutations from the genome. Theory predicts that transitions to asexuality should lead to the suppression of recombination and segregation and, in turn, weakened natural selection, allowing for the accumulation of slightly deleterious mutations. We tested this prediction by estimating the d<em>N</em>/d<em>S</em> ratios in asexual vertebrate lineages in the genus <em>Aspidoscelis</em> using whole mitochondrial genomes from seven asexual and five sexual species. We found higher d<em>N</em>/d<em>S</em> ratios in asexual <em>Aspidoscelis </em>species, indicating that asexual whiptails accumulate non-synonymous substitutions due to weaker purifying selection. Additionally, we estimated nucleotide diversity and found that asexuals harbor significantly less diversity. Thus, despite their recent origins, slightly deleterious mutations accumulated rapidly enough in asexual lineages to be detected. We provided empirical evidence to corroborate the connection between asexuality and increased </span><span>amino acid substitutions</span><span> in asexual vertebrate lineages.</span></p> <p class="MsoNormal"><span> </span></p>
Two type I topoisomerases maintain DNA topology in human mitochondria
<p>Raw image data from the article "Two type I topoisomerases maintain DNA topology in human mitochondria" by Katja E. Menger et al.</p>
Fig. 5. Compound 7 induced apoptosis through a mitochondria-dependent pathway. A in Bufadienolide glycosides and bufadienolides from the whole plants of Helleborus lividus, and their cytotoxic activity
Fig. 5. Compound 7 induced apoptosis through a mitochondria-dependent pathway. A, Mitochondrial membrane morphology of HL- 60 cells treated with 7. HL-60 cells were stained with MitoCapture™ reagent after treatment with either 0.21 μM of 7 or 33 μM of cisplatin for 6 h and observed under a fluorescence microscope. B, Release of cytochrome c from mitochondria of HL-60 cells treated with 7. HL-60 cells were treated with either 0.21 μM of 7 or 33 μM of cisplatin for 8 h, and the release of cytochrome c into the cytoplasm was evaluated by Western blot analysis.
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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.