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Marine amebae of the genus Paramoeba (Amoebozoa, Dactylopodida) normally contain a eukaryotic endosymbiont known as Perkinsela-like organism (PLO). This is one of the characters to distinguish the genera Neoparamoeba and Paramoeba...
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Marine amebae of the genus Paramoeba (Amoebozoa, Dactylopodida) normally contain a eukaryotic endosymbiont known as Perkinsela-like organism (PLO). This is one of the characters to distinguish the genera Neoparamoeba and Paramoeba from other Dactylopodida. It is known that the PLO may be lost, but PLO-free strains of paramoebians were never available for molecular studies. Recently, we have described the first species of the genus Paramoeba which has no parasome-Paramoeba aparasomata. In this study, we present a mitochondrial genome of this species, compare it with that of Neoparamoeba pemaquidensis, and analyze the evolutionary dynamics of gene sequences and gene order rearrangements between these species. The mitochondrial genome of P. aparasomata is 46,254 bp long and contains a set of 31 protein-coding genes, 19 tRNAs, two rRNA genes, and 7 open reading frames. Our results suggest that these two mitochondrial genomes within the genus Paramoeba have rather similar organization and gene order, base composition, codon usage, the composition and structure of noncoding, and overlapping regions.
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Mitochondria play an essential part in fighting against pathogen infection in the defense responses of fruits. In this study, we investigated the reactive oxygen species (ROS) production, energy metabolism, and changes of mitochon...
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Mitochondria play an essential part in fighting against pathogen infection in the defense responses of fruits. In this study, we investigated the reactive oxygen species (ROS) production, energy metabolism, and changes of mitochondrial proteins in harvested muskmelon fruits (Cucumis melo cv. Yujinxiang) inoculated with Trichothecium roseum. The results indicated that the fungal infection obviously induced the H2O2 accumulation in mitochondria. Enzyme activities were inhibited in the first 6 h postinoculation (hpi), including succinic dehydrogenase, cytochrome c oxidase, H+-ATPase, and Ca2+-ATPase. However, the activities of Ca2+-ATPase and 11+-ATPase and the contents of intracellular adenosine triphosphate (ATP) were improved to a higher level at 12 hpi. A total of 42 differentially expressed proteins were identified through tandem mass tagsbased proteomic analyses, which are mainly involved in energy metabolism, stress responses and redox homeostasis, glycolysis and tricarboxylic acid cycle, and transporter and mitochondria dysfunction. Taken together, our results suggest that mitochondria play crucial roles in the early defense responses of muskmelons against T. roseum infection through regulation of ROS production and energy metabolism.
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Mitochondrial activity and cell energy status play important roles in the regulation of cell cycle and cell proliferation. Regulation of mitochondrial gene expression is crucial for mitochondrial activity regulation. The mitochond...
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Mitochondrial activity and cell energy status play important roles in the regulation of cell cycle and cell proliferation. Regulation of mitochondrial gene expression is crucial for mitochondrial activity regulation. The mitochondrial transcription termination factor (MTERF) family is a group of important mitochondrial transcription regulatory factors. It has been demonstrated that MTERF1–3 are involved in the regulation of mitochondrial gene transcription and oxidative phosphorylation. However, the function of the newest member MTERF4 has not been characterized. In this study, human MTERF4 full-length open reading frame was cloned, and the protein structure prediction revealed that hMTERF4 protein contained leucine-zipper motifs, which is similar to human MTERF1–3. The expressed pMTERF4-green fluorescence fusion protein in HeLa cells localized the mitochondria. (3(4,5)dimethylthiahiazo(zy1)3,5diphenytetrazoliumromide) (MTT) proliferation assay and flow cytometry analysis showed that hMTERF4 knockdown induced sub-G1 phase cells accumulation, whereas its overexpression promoted cell proliferation. Furthermore, double staining with Annexin V and PI revealed that hMTERF4 knockdown increased necrosis but not apoptosis. In conclusion, our data suggested that hMTERF4 is an essential factor for cell proliferation, which is probably modulated by mitochondrial transcription to promote cell proliferation.
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To obtain a comprehensive understanding of proteins involved in mitochondrion-sarcoplasmic reticulum (SR) linking, a catalog of proteins from mitochondrion-associated membrane (MAM) of New Zealand white rabbit skeletal muscle were...
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To obtain a comprehensive understanding of proteins involved in mitochondrion-sarcoplasmic reticulum (SR) linking, a catalog of proteins from mitochondrion-associated membrane (MAM) of New Zealand white rabbit skeletal muscle were analyzed by an optimized shotgun proteomic method. The membrane fractions were prepared by differential centrifugation and separated by 1D electrophoresis followed by a highly reproducible, automated LC-MS/MS on the hybrid linear ion trap (LTQ)-Orbitrap mass spectrometer. By integrating as low as 1% false discovery rate as one of the features for quality control method, 459 proteins were identified from both of the two independent MAM preparations. Protein pI value, molecular weight range, and transmembrane region were calculated using bioinformatics softwares. One hundred one proteins were recognized as membrane proteins. This protein database suggested that the MAM preparations composed of proteins from mitochondrion, SR, and transverse-tubule. This result indicated mitochondria physically linked with SR in rabbit skeletal muscle, voltage-dependent anion channel 1 (VDAC1), VDAC2, and VDAC3 might participate in formation of the tethers between SR and mitochondria.
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Mitochondrial dysfunction has been implicated in the aetiology of many complex diseases, as well as the ageing process. Much of the research on mitochondrial dysfunction has focused on how mitochondrial damage may potentiate patho...
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Mitochondrial dysfunction has been implicated in the aetiology of many complex diseases, as well as the ageing process. Much of the research on mitochondrial dysfunction has focused on how mitochondrial damage may potentiate pathological phenotypes. The purpose of this review is to draw attention to the less well-studied mechanisms by which the cell adapts to mitochondrial perturbations. This involves communication of stress to the cell and successful induction of quality control responses,which include mitophagy, unfolded protein response, upregulation of antioxidant andDNA repair enzymes, morphological changes, and if all else fails apoptosis. The mitochondrion is an inherently stressful environment and we speculate that dysregulation of stress signaling or an inability to switch on these adaptations during times of mitochondrial stress may underpin mitochondrial dysfunction and hence amount to pathological states over time.
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Mitochondria are essential organelles within the cell where most of the energy production occurs by the oxidative phosphorylation system (OXPHOS). Critical components of the OXPHOS are encoded by the mitochondrial DNA (mtDNA) and ...
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Mitochondria are essential organelles within the cell where most of the energy production occurs by the oxidative phosphorylation system (OXPHOS). Critical components of the OXPHOS are encoded by the mitochondrial DNA (mtDNA) and therefore, mutations involving this genome can be deleterious to the cell. Post-mitotic tissues, such as muscle and brain, are most sensitive to mtDNA changes, due to their high energy requirements and non-proliferative status. It has been proposed that mtDNA biological features and location make it vulnerable to mutations, which accumulate over time. However, although the role of mtDNA damage has been conclusively connected to neuronal impairment in mitochondrial diseases, its role in age-related neurodegenerative diseases remains speculative. Here we review the pathophysiology of mtDNA mutations leading to neurodegeneration and discuss the insights obtained by studying mouse models of mtDNA dysfunction. This article is part of a Special Issue entitled: Misfolded Proteins, Mitochondrial Dysfunction, and Neurodegenerative Diseases. (C) 2013 Published by Elsevier B.V.
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Recent studies on patients with sporadic ALS and on in vitro and in vivo models of mendelian diseases have been addressed toward the unravelling of the mitochondrial behaviour in ALS, whether as a primarily pathogenic factor, or a...
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Recent studies on patients with sporadic ALS and on in vitro and in vivo models of mendelian diseases have been addressed toward the unravelling of the mitochondrial behaviour in ALS, whether as a primarily pathogenic factor, or as a fundamental contributor to the cell death. Morphological evidence suggests mitochondria pathology in ALS and many physiological mechanisms involving these organelles appear deranged in ALS, such as energy production, apoptotic triggering, calcium homeostasis and axonal transport of mitochondria. The article briefly addresses recent advances on this field.
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We present data on mitochondrial DNA deletions and mitochondrial diseases. The mechanism of their occurrence is discussed on the basis of deletion breakpoints and particularly with the slippage mispairing hypothesis. As the correl...
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We present data on mitochondrial DNA deletions and mitochondrial diseases. The mechanism of their occurrence is discussed on the basis of deletion breakpoints and particularly with the slippage mispairing hypothesis. As the correlation between the genotypes and the phenotypes is not always straightforward, a classification of mitochondrial diseases is suggested according to the genotype (deletions, depletions and duplications, mutations affecting structural genes or tRNA genes) rather than the phenotype. The effect of mitochondrial DNA alterations on the expression of nuclear encoded proteins is presented, and the nucleus can be found to respond differently but in a coordinate way according to the kind of mitochondrial DNA alteration. The search for a nuclear gene affecting the expression of Leber's disease could not show any correlation between the alleles of TAP2 (transporter antigen peptide) and the expression of the disease. Finally, we present new data on another class of myopathies, namely Duchenne muscular dystrophy (DMD), where mitochondria could play an unexpected role in the metabolism of calcium. In some patients with DMD a mitochondrial calcium binding protein that is mainly located in the mitochondrial matrix and which is named "calmitine" was found to disappear. We have thus cloned its cDNA and found that it was identical with to calsequestrine which is a high-capacity but low-affinity Ca2+ binding protein from the sarcoplasmic reticulum.
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We reported the complete mitochondrial genome sequencing of a important hypertension model inbred rat strain for the first time. The total length of the mitogenome was 16,310 bp. It harbored 13 protein-coding genes, 2 ribosomal RN...
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We reported the complete mitochondrial genome sequencing of a important hypertension model inbred rat strain for the first time. The total length of the mitogenome was 16,310 bp. It harbored 13 protein-coding genes, 2 ribosomal RNA genes, 22 transferRNA genes and1 non-coding control region. The mutation events contained in this strain were also reported.
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We sequenced the complete mitochondrial genome sequencing of an important melanoma disease model inbred rat strain for the first time. The total length of the mitogenome was 16,309bp and coding 13 protein-coding genes, 2 ribosomal...
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We sequenced the complete mitochondrial genome sequencing of an important melanoma disease model inbred rat strain for the first time. The total length of the mitogenome was 16,309bp and coding 13 protein-coding genes, 2 ribosomal RNA genes, 22 transferRNA genes.
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