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Mitochondrial respiration

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https://www.readbyqxmd.com/read/28214511/identification-of-a-degradation-signal-sequence-within-substrates-of-the-mitochondrial-i-aaa-protease
#1
Anthony J Rampello, Steven E Glynn
The i-AAA protease is a component of the mitochondrial quality control machinery that regulates respiration, mitochondrial dynamics, and protein import. The protease is required to select specific substrates for degradation from among the diverse complement of proteins present in mitochondria, yet the rules that govern this selection are unclear. Here, we reconstruct the yeast i-AAA protease, Yme1p, to examine the in vitro degradation of two intermembrane space chaperone subunits, Tim9 and Tim10. Yme1p degrades Tim10 more rapidly than Tim9 despite high sequence and structural similarity, and loss of Tim10 is accelerated by disruption of conserved disulfide bonds within the substrate...
February 15, 2017: Journal of Molecular Biology
https://www.readbyqxmd.com/read/28213476/editing-of-mitochondrial-transcripts-nad3-and-cox2-by-dek10-is-essential-for-mitochondrial-function-and-maize-plant-development
#2
Weiwei Qi, Zhongrui Tian, Lei Lu, Xiuzu Chen, Xinze Chen, Wei Zhang, Rentao Song
Respiration, the core of mitochondrial metabolism, depends on the function of five respiratory complexes. Many respiratory chain related proteins are encoded by the mitochondrial genome and their RNAs undergo post-transcriptional modifications by nuclear genome expressed factors, including pentatricopeptide repeat (PPR) proteins. Maize defective kernel 10 (dek10) is a classic mutant with small kernels and delayed development. Through positional cloning we found that Dek10 encodes an E-subgroup PPR protein localized in mitochondria...
February 17, 2017: Genetics
https://www.readbyqxmd.com/read/28207742/narciclasine-attenuates-diet-induced-obesity-by-promoting-oxidative-metabolism-in-skeletal-muscle
#3
Sofi G Julien, Sun-Yee Kim, Reinhard Brunmeir, Joanna R Sinnakannu, Xiaojia Ge, Hongyu Li, Wei Ma, Jadegoud Yaligar, Bhanu Prakash Kn, Sendhil S Velan, Pia V Röder, Qiongyi Zhang, Choon Kiat Sim, Jingyi Wu, Marta Garcia-Miralles, Mahmoud A Pouladi, Wei Xie, Craig McFarlane, Weiping Han, Feng Xu
Obesity develops when caloric intake exceeds metabolic needs. Promoting energy expenditure represents an attractive approach in the prevention of this fast-spreading epidemic. Here, we report a novel pharmacological strategy in which a natural compound, narciclasine (ncls), attenuates diet-induced obesity (DIO) in mice by promoting energy expenditure. Moreover, ncls promotes fat clearance from peripheral metabolic tissues, improves blood metabolic parameters in DIO mice, and protects these mice from the loss of voluntary physical activity...
February 2017: PLoS Biology
https://www.readbyqxmd.com/read/28206987/id2-promotes-survival-of-glioblastoma-cells-during-metabolic-stress-by-regulating-mitochondrial-function
#4
Zhonghua Zhang, Gilbert J Rahme, Pranam D Chatterjee, Matthew C Havrda, Mark A Israel
Tumor cells proliferate in cellular environments characterized by a lack of optimal tissue organization resulting oftentimes in compromised cellular metabolism affecting nutrition, respiration, and energetics. The response of tumor cells to adverse environmental conditions is a key feature affecting their pathogenicity. We found that inhibitor of DNA binding 2 (ID2) expression levels significantly correlate with the ability of glioblastoma (GBM)-derived cell lines to survive glucose deprivation. ID2 suppressed mitochondrial oxidative respiration and mitochondrial ATP production by regulating the function of mitochondrial electron transport chain (mETC) complexes, resulting in reduced superoxide and reactive oxygen species (ROS) production from mitochondria...
February 16, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28205616/dependence-on-glycolysis-sensitizes-braf-mutated-melanomas-for-increased-response-to-targeted-braf-inhibition
#5
Keisha N Hardeman, Chengwei Peng, Bishal B Paudel, Christian T Meyer, Thong Luong, Darren R Tyson, Jamey D Young, Vito Quaranta, Joshua P Fessel
Dysregulated metabolism can broadly affect therapy resistance by influencing compensatory signaling and expanding proliferation. Given many BRAF-mutated melanoma patients experience disease progression with targeted BRAF inhibitors, we hypothesized therapeutic response is related to tumor metabolic phenotype, and that altering tumor metabolism could change therapeutic outcome. We demonstrated the proliferative kinetics of BRAF-mutated melanoma cells treated with the BRAF inhibitor PLX4720 fall along a spectrum of sensitivity, providing a model system to study the interplay of metabolism and drug sensitivity...
February 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28205519/mitochondrial-atp-transporter-depletion-protects-mice-against-liver-steatosis-and-insulin-resistance
#6
Joonseok Cho, Yujian Zhang, Shi-Young Park, Anna-Maria Joseph, Chul Han, Hyo-Jin Park, Srilaxmi Kalavalapalli, Sung-Kook Chun, Drake Morgan, Jae-Sung Kim, Shinichi Someya, Clayton E Mathews, Young Jae Lee, Stephanie E Wohlgemuth, Nishanth E Sunny, Hui-Young Lee, Cheol Soo Choi, Takayuki Shiratsuchi, S Paul Oh, Naohiro Terada
Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disorder in obese individuals. Adenine nucleotide translocase (ANT) exchanges ADP/ATP through the mitochondrial inner membrane, and Ant2 is the predominant isoform expressed in the liver. Here we demonstrate that targeted disruption of Ant2 in mouse liver enhances uncoupled respiration without damaging mitochondrial integrity and liver functions. Interestingly, liver specific Ant2 knockout mice are leaner and resistant to hepatic steatosis, obesity and insulin resistance under a lipogenic diet...
February 16, 2017: Nature Communications
https://www.readbyqxmd.com/read/28202542/m%C3%A3-ssbauer-spectra-of-mouse-hearts-reveal-age-dependent-changes-in-mitochondrial-and-ferritin-iron-levels
#7
Joshua D Wofford, Mrinmoy Chakrabarti, Paul Alan Lindahl
Cardiac function requires continuous high levels of energy, and so iron, a critical player in mitochondrial respiration, is an important component of the heart. Hearts from (57)Fe-enriched mice were evaluated by Mossbauer spectroscopy. Spectra consisted of a sextet and two quadrupole doublets. One doublet was due to residual blood while the other was due to [Fe4S4](2+) clusters and Fe(II) hemes, most of which were associated with mitochondrial respiration. The sextet was due to ferritin; there was no evidence of hemosiderin, a ferritin decomposition product...
February 15, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28202494/fumarate-hydratase-is-a-critical-metabolic-regulator-of-hematopoietic-stem-cell-functions
#8
Amelie V Guitart, Theano I Panagopoulou, Arnaud Villacreces, Milica Vukovic, Catarina Sepulveda, Lewis Allen, Roderick N Carter, Louie N van de Lagemaat, Marcos Morgan, Peter Giles, Zuzanna Sas, Marta Vila Gonzalez, Hannah Lawson, Jasmin Paris, Joy Edwards-Hicks, Katrin Schaak, Chithra Subramani, Deniz Gezer, Alejandro Armesilla-Diaz, Jimi Wills, Aaron Easterbrook, David Coman, Chi Wai Eric So, Donal O'Carroll, Douglas Vernimmen, Neil P Rodrigues, Patrick J Pollard, Nicholas M Morton, Andrew Finch, Kamil R Kranc
Strict regulation of stem cell metabolism is essential for tissue functions and tumor suppression. In this study, we investigated the role of fumarate hydratase (Fh1), a key component of the mitochondrial tricarboxylic acid (TCA) cycle and cytosolic fumarate metabolism, in normal and leukemic hematopoiesis. Hematopoiesis-specific Fh1 deletion (resulting in endogenous fumarate accumulation and a genetic TCA cycle block reflected by decreased maximal mitochondrial respiration) caused lethal fetal liver hematopoietic defects and hematopoietic stem cell (HSC) failure...
February 15, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/28195532/horizontal-transfer-of-whole-mitochondria-restores-tumorigenic-potential-in-mitochondrial-dna-deficient-cancer-cells
#9
Lan-Feng Dong, Jaromira Kovarova, Martina Bajzikova, Ayenachew Bezawork-Geleta, David Svec, Berwini Endaya, Karishma Sachaphibulkij, Ana R Coelho, Natasa Sebkova, Anna Ruzickova, An S Tan, Katarina Kluckova, Kristyna Judasova, Katerina Zamecnikova, Zuzana Rychtarcikova, Vinod Gopalan, Margaryta Sobol, Bing Yan, Bijay Pattnaik, Naveen Bhatraju, Jaroslav Truksa, Pavel Stopka, Pavel Hozak, Alfred Lam, Radislav Sedlacek, Paulo J Oliveira, Mikael Kubista, Anurag Agrawal, Katerina Dvorakova-Hortova, Jakub Rohlena, Michael V Berridge, Jiri Neuzil
Recently we showed that generation of tumours in syngeneic mice by cells devoid of mitochondrial (mt) DNA (ρ(0) cells) is linked to acquisition of the host mtDNA. However, the mechanism of mtDNA movement between cells remains unresolved. To determine whether transfer of mtDNA involves whole mitochondria, we injected B16ρ(0) mouse melanoma cells into syngeneic C57BL/6N(su9-DsRed2) mice that express red fluorescent protein in their mitochondria. We document that mtDNA is acquired by transfer of whole mitochondria from the host animal, leading to normalisation of mitochondrial respiration...
February 14, 2017: ELife
https://www.readbyqxmd.com/read/28193887/tmem175-deficiency-impairs-lysosomal-and-mitochondrial-function-and-increases-%C3%AE-synuclein-aggregation
#10
Sarah Jinn, Robert E Drolet, Paige E Cramer, Andus Hon-Kit Wong, Dawn M Toolan, Cheryl A Gretzula, Bhavya Voleti, Galya Vassileva, Jyoti Disa, Marija Tadin-Strapps, David J Stone
Parkinson disease (PD) is a neurodegenerative disorder pathologically characterized by nigrostriatal dopamine neuron loss and the postmortem presence of Lewy bodies, depositions of insoluble α-synuclein, and other proteins that likely contribute to cellular toxicity and death during the disease. Genetic and biochemical studies have implicated impaired lysosomal and mitochondrial function in the pathogenesis of PD. Transmembrane protein 175 (TMEM175), the lysosomal K(+) channel, is centered under a major genome-wide association studies peak for PD, making it a potential candidate risk factor for the disease...
February 13, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28191887/the-creatine-kinase-pathway-is-a-metabolic-vulnerability-in-evi1-positive-acute-myeloid-leukemia
#11
Nina Fenouille, Christopher F Bassil, Issam Ben-Sahra, Lina Benajiba, Gabriela Alexe, Azucena Ramos, Yana Pikman, Amy S Conway, Michael R Burgess, Qing Li, Frédéric Luciano, Patrick Auberger, Ilene Galinsky, Daniel J DeAngelo, Richard M Stone, Yi Zhang, Archibald S Perkins, Kevin Shannon, Michael T Hemann, Alexandre Puissant, Kimberly Stegmaier
Expression of the MECOM (also known as EVI1) proto-oncogene is deregulated by chromosomal translocations in some cases of acute myeloid leukemia (AML) and is associated with poor clinical outcome. Here, through transcriptomic and metabolomic profiling of hematopoietic cells, we reveal that EVI1 overexpression alters cellular metabolism. A screen using pooled short hairpin RNAs (shRNAs) identified the ATP-buffering, mitochondrial creatine kinase CKMT1 as necessary for survival of EVI1-expressing cells in subjects with EVI1-positive AML...
February 13, 2017: Nature Medicine
https://www.readbyqxmd.com/read/28188211/cluh-regulates-mitochondrial-metabolism-by-controlling-translation-and-decay-of-target-mrnas
#12
Désirée Schatton, David Pla-Martin, Marie-Charlotte Marx, Henriette Hansen, Arnaud Mourier, Ivan Nemazanyy, Alberto Pessia, Peter Zentis, Teresa Corona, Vangelis Kondylis, Esther Barth, Astrid C Schauss, Vidya Velagapudi, Elena I Rugarli
Mitochondria are essential organelles that host crucial metabolic pathways and produce adenosine triphosphate. The mitochondrial proteome is heterogeneous among tissues and can dynamically change in response to different metabolic conditions. Although the transcriptional programs that govern mitochondrial biogenesis and respiratory function are well known, posttranscriptional regulatory mechanisms remain unclear. In this study, we show that the cytosolic RNA-binding protein clustered mitochondria homologue (CLUH) regulates the expression of a mitochondrial protein network supporting key metabolic programs required under nutrient deprivation...
February 10, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28186163/label-free-detection-of-myocardial-ischaemia-in-the-perfused-rat-heart-by-spontaneous-raman-spectroscopy
#13
Suguru Ohira, Hideo Tanaka, Yoshinori Harada, Takeo Minamikawa, Yasuaki Kumamoto, Satoaki Matoba, Hitoshi Yaku, Tetsuro Takamatsu
Raman spectroscopy, which identifies intrinsic molecular constituents, has a potential for determining myocardial viability under label-free conditions. However, its suitability for evaluating myocardial ischaemia is undetermined. Focusing on cytochromes, i.e., representative molecules reflecting mitochondrial activity, we tested whether Raman spectroscopy is applicable for evaluating myocardial ischaemia especially during early ischaemic phase. We obtained spontaneous Raman spectra of the subepicardial myocardium in the Langendorff-perfused rat heart upon 532-nm excitation before and during the "stopped-flow," global ischaemia...
February 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28183803/hexokinase-ii-derived-cell-penetrating-peptide-targets-mitochondria-and-triggers-apoptosis-in-cancer-cells
#14
Abiy D Woldetsadik, Maria C Vogel, Wael M Rabeh, Mazin Magzoub
Overexpression of mitochondria-bound hexokinase II (HKII) in cancer cells plays an important role in their metabolic reprogramming and protects them against apoptosis, thereby facilitating their growth and proliferation. Here, we show that covalently coupling a peptide that corresponds to the mitochondrial membrane-binding N-terminal domain of HKII (pHK) to a short, penetration-accelerating sequence (PAS) enhances the cellular uptake, mitochondrial localization, and cytotoxicity of the peptide in HeLa cells...
February 9, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28181692/irisin-plays-a-pivotal-role-to-protect-the-heart-against-ischemia-and-reperfusion-injury
#15
Hao Wang, Yu Tina Zhao, Shouyan Zhang, Patrycja M Dubielecka, Jianfeng Du, Naohiro Yano, Y Eugene Chin, Shougang Zhuang, Gangjian Qin, Ting C Zhao
Irisin, a newly identified hormone, is critical to modulating body metabolism, thermogenesis and reducing oxidative stresses. However, whether irisin protects the heart against myocardial ischemia and reperfusion (I/R) injury remains unknown. In this study, we determine the effect of irisin on myocardial I/R injury in the Langendorff perfused heart and cultured myocytes. Adult C57/BL6 mice were treated with irisin (100mg/kg) or vehicle for 30 minutes to elicit preconditioning. The isolated hearts were subjected to 30 min ischemia followed by 30 min reperfusion...
February 9, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28179093/sorafenib-and-fh535-in-combination-act-synergistically-on-hepatocellular-carcinoma-by-targeting-cell-bioenergetics-and-mitochondrial-function
#16
Lilia Turcios, Valery Vilchez, Luis F Acosta, Pratheeshkumar Poyil, David Allan Butterfield, Mihail Mitov, Francesc Marti, Roberto Gedaly
Treatment of advanced hepatocellular carcinoma (HCC) remains a challenge due to the high tumor heterogeneity. In the present study, we aim to evaluate the impact of the β-catenin inhibitor, FH535, alone or in combination with the Ras/Raf/MAPK inhibitor Sorafenib, on the bioenergetics profiles of the HCC cell lines Huh7 and PLC/PRF/5. Single low-dose treatments with FH535 or Sorafenib promoted different effects on mitochondrial respiration and glycolysis in a cell type specific manner. However, the combination of these drugs significantly reduced both mitochondrial respiration and glycolytic rates regardless of the HCC cells...
January 19, 2017: Digestive and Liver Disease
https://www.readbyqxmd.com/read/28176017/hypoxia-and-aerobic-metabolism-adaptations-of-human-endothelial-cells
#17
Agnieszka Koziel, Wieslawa Jarmuszkiewicz
The goal of our study was to assess the influence of chronic exposure to hypoxia on mitochondrial oxidative metabolism in human umbilical vein endothelial cells (EA.hy926 line) cultured for 6 days at 1% O2 tension. The hypoxia-induced effects were elucidated at the cellular and isolated mitochondria levels. Hypoxia elevated fermentation but did not change mitochondrial biogenesis or the aerobic respiratory capacity of endothelial cells. In endothelial cells, hypoxia caused a general decrease in mitochondrial respiration during carbohydrate, fatty acid, and amino acid oxidation but increased exclusively ketogenic amino acid oxidation...
February 8, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/28174288/direct-substrate-delivery-into-mitochondrial-fission-deficient-pancreatic-islets-rescues-insulin-secretion
#18
Uma D Kabra, Katrin Pfuhlmann, Adriana Migliorini, Susanne Keipert, Daniel Lamp, Olle Korsgren, Moritz Gegg, Stephen C Woods, Paul T Pfluger, Heiko Lickert, Charles Affourtit, Matthias H Tschöp, Martin Jastroch
In pancreatic beta cells, mitochondrial bioenergetics control glucose-stimulated insulin secretion (GSIS). Mitochondrial dynamics are generally associated with quality control, maintaining the functionality of bioenergetics. By acute pharmacological inhibition of mitochondrial fission protein Drp1, we here demonstrate that mitochondrial fission is necessary for GSIS in mouse and human islets. We confirm that genetic silencing of Drp1 increases mitochondrial proton leak in MIN6 cells. However, our comprehensive analysis of pancreatic islet bioenergetics reveals that Drp1 does not control insulin secretion via its effect on proton leak but instead via modulation of glucose-fuelled respiration...
February 7, 2017: Diabetes
https://www.readbyqxmd.com/read/28174208/l-opa1-regulates-mitoflash-biogenesis-independently-from-membrane-fusion
#19
Manon Rosselin, Jaime Santo-Domingo, Flavien Bermont, Marta Giacomello, Nicolas Demaurex
Mitochondrial flashes mediated by optic atrophy 1 (OPA1) fusion protein are bioenergetic responses to stochastic drops in mitochondrial membrane potential (Δψm) whose origin is unclear. Using structurally distinct genetically encoded pH-sensitive probes, we confirm that flashes are matrix alkalinization transients, thereby establishing the pH nature of these events, which we renamed "mitopHlashes". Probes located in cristae or intermembrane space as verified by electron microscopy do not report pH changes during Δψm drops or respiratory chain inhibition...
February 7, 2017: EMBO Reports
https://www.readbyqxmd.com/read/28168604/the-natural-product-osthole-attenuates-yeast-growth-by-extensively-suppressing-the-gene-expressions-of-mitochondrial-respiration-chain
#20
Zhe Wang, Yan Shen
The fast growing evidences have indicated that the natural product osthole is a promising drug candidate for fighting several serious human diseases, for example, cancer and inflammation. However, the mode-of-action (MoA) of osthole remains largely incomplete. In this study, we investigated the growth inhibition activity of osthole using fission yeast as a model, with the goal of understanding the osthole's mechanism of action, especially from the molecular level. Microarray analysis indicated that osthole has significant impacts on gene transcription levels (In total, 214 genes are up-regulated, and 97 genes are down-regulated)...
February 7, 2017: Current Microbiology
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