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The FEBS Journal

Cover image for Vol. 280 Issue 20

October 2013

Volume 280, Issue 20

Pages i–iii, 4931–5161

  1. Front Cover

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Editorial
    5. Focus on Mitochondria Series
    6. Original Articles
    7. Author index
    8. Table of Contents
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      Front Cover (page i)

      Version of Record online: 1 OCT 2013 | DOI: 10.1111/j.1742-4658.2013.08798.x

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      Ischaemia/reperfusion can induce mitochondrial dysfunction and apoptosis via cytochrome c release (from Borutaite et al. pp. 4999–5014 with background ‘Mitochondria in action’ by Odra Noel www.odranoel.eu).

  2. Editorial Information

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Editorial
    5. Focus on Mitochondria Series
    6. Original Articles
    7. Author index
    8. Table of Contents
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      Editorial Information (pages ii–iii)

      Version of Record online: 1 OCT 2013 | DOI: 10.1111/j.1742-4658.2013.08798_1.x

  3. Editorial

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Editorial
    5. Focus on Mitochondria Series
    6. Original Articles
    7. Author index
    8. Table of Contents
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      Prizes awarded by FEBS Journal and FEBS Letters from 2015 (page 4931)

      Richard Perham and Felix Wieland

      Version of Record online: 30 SEP 2013 | DOI: 10.1111/febs.12527

  4. Focus on Mitochondria Series

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Editorial
    5. Focus on Mitochondria Series
    6. Original Articles
    7. Author index
    8. Table of Contents
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      Introduction: Focus on mitochondria (page 4932)

      Kostas Tokatlidis and Guy C. Brown

      Version of Record online: 23 SEP 2013 | DOI: 10.1111/febs.12504

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      This is a series of papers (three reviews and five regular papers) focused on Mitochondria from authors contributing to two FEBS courses on Mitochondria held in 2012. These papers focus on: (i) mitochondrial biogenesis (regulation by phosphorylation, import of SOD1 and Mia40, mitophagy and tRNA variants) or (ii) mitochondrial pathology (ischaemia, obesity and Parkinson's disease).

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      From inventory to functional mechanisms : Regulation of the mitochondrial protein import machinery by phosphorylation (pages 4933–4942)

      Carolin Gerbeth, Despina Mikropoulou and Chris Meisinger

      Version of Record online: 19 AUG 2013 | DOI: 10.1111/febs.12445

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      Mitochondrial protein import machineries and import pathways have been studied in great detail. However, mechanisms that regulate the protein import machineries were largely unexplored. Here, we review recent findings on the discovery of regulatory principles of the central mitochondrial protein entry gate TOM that is phosphorylated by cytosolic kinases.

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      Mia40 and MINOS act in parallel with Ccs1 in the biogenesis of mitochondrial Sod1 (pages 4943–4959)

      Aksana Varabyova, Ulrike Topf, Paulina Kwiatkowska, Lidia Wrobel, Magdalena Kaus-Drobek and Agnieszka Chacinska

      Version of Record online: 22 JUL 2013 | DOI: 10.1111/febs.12409

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      Sod1 is a superoxide-scavenging enzyme in the cytosol and intermembrane space of mitochondria. We created yeast mutants in conserved amino acid residues responsible for amyotrophic lateral sclerosis. The pathogenic Sod1 forms were present in the intermembrane space of mitochondria. We identified mitochondrial players, Mia40 and mitochondrial inner membrane organizing system (MINOS), that affect the mitochondrial localization of pathogenic Sod1 variants.

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      Biogenesis of yeast Mia40 – uncoupling folding from import and atypical recognition features (pages 4960–4969)

      Afroditi Chatzi, Dionisia P. Sideris, Nitsa Katrakili, Charalampos Pozidis and Kostas Tokatlidis

      Version of Record online: 2 SEP 2013 | DOI: 10.1111/febs.12482

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      A stepwise model for the yeast Mia40 biogenesis in mitochondria. The mechanism requires crossing via the TOM complex, followed by insertion through the TIM23 translocon. The interaction with endogenous Mia40 drives folding of the protein core and allows oxidation of the CPC motif by Erv1. Different determinants guide each step to complete the assembly of Mia40 in the IMS.

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      Uth1 is a mitochondrial inner membrane protein dispensable for post-log-phase and rapamycin-induced mitophagy (pages 4970–4982)

      Evelyn Welter, Marco Montino, Robert Reinhold, Petra Schlotterhose, Roswitha Krick, Jan Dudek, Peter Rehling and Michael Thumm

      Version of Record online: 2 SEP 2013 | DOI: 10.1111/febs.12468

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      We compared the mitophagy rate and requirement for mitophagy-specific proteins during post-log-phase and rapamycin-induced mitophagy. To assess mitophagy of damaged mitochondria, we analyzed cells lacking the mitochondrial AAA-protease Yme1. Unexpectedly, we found that Uth1 was dispensable for mitophagy and that it is a protein of the inner mitochondrial membrane that is targeted by a cleavable N-terminal pre-sequence.

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      Length variation in the mouse mitochondrial tRNAArg DHU loop size promotes oxidative phosphorylation functional differences (pages 4983–4998)

      Raquel Moreno-Loshuertos, Acisclo Pérez-Martos, Patricio Fernández-Silva and José Antonio Enríquez

      Version of Record online: 2 SEP 2013 | DOI: 10.1111/febs.12466

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      The OXPHOS system efficiency is modulated by common mitochondrial tRNAArg haplotypes affecting the mature tRNA DHU loop. We demonstrate that it is the tRNA loop size what induces differences in cellular respiration and promotes differential sensitivity to mitochondrial translation specific inhibitors. We also confirm that these differences are masked by a ROS-induced compensatory increase in mitochondrial biogenesis.

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      In the eye of the storm: mitochondrial damage during heart and brain ischaemia (pages 4999–5014)

      Vilmante Borutaite, Adolfas Toleikis and Guy C. Brown

      Version of Record online: 18 JUN 2013 | DOI: 10.1111/febs.12353

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      Mitochondria are at the center of ischaemic damage to heart and brain. Here, we highlight the mechanisms and consequences of early events in mitochondrial ischaemic damage, particularly complex I inhibition and the release of cytochrome c from mitochondria, and discuss how inhibition of mitochondria by nitric oxide may contribute to ischaemic injury to heart and brain.

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      Implications of mitochondrial uncoupling in skeletal muscle in the development and treatment of obesity (pages 5015–5029)

      A. Brianne Thrush, Robert Dent, Ruth McPherson and Mary-Ellen Harper

      Version of Record online: 12 JUL 2013 | DOI: 10.1111/febs.12399

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      Understanding the metabolic factors that contribute to obesity and weight loss are critical for combating obesity and obesity related disorders. Here, we discuss how mitochondrial proton leak contributes to energy expenditure. We provide evidence to support the hypothesis that differences in oxidative phosphorylation efficiency contribute to inter-individual variation in weight loss success.

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      Rotenone induces neuronal death by microglial phagocytosis of neurons (pages 5030–5038)

      Julius V. Emmrich, Tamara C. Hornik, Jonas J. Neher and Guy C. Brown

      Version of Record online: 10 JUL 2013 | DOI: 10.1111/febs.12401

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      We report that rotenone induced neuronal loss in mixed neuronal/glial cultures without increasing the number of necrotic or apoptotic neurons. Neuronal loss could be prevented by inhibition of phagocytic signalling between neurons and microglia. This indicates that rotenone toxicity is at least partially mediated by microglial phagocytosis of otherwise viable neurons (phagoptosis).

  5. Original Articles

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Editorial
    5. Focus on Mitochondria Series
    6. Original Articles
    7. Author index
    8. Table of Contents
    1. You have free access to this content
      Identification of key amino acid residues in the catalytic mechanism of diaminopropionate ammonialyase from Salmonella typhimurium (pages 5039–5051)

      Josyula N. Kalyani, Shveta Bisht, Mariyanna Lakshmikanth, Mathur R. N. Murthy and Handanahal S. Savithri

      Version of Record online: 2 SEP 2013 | DOI: 10.1111/febs.12474

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      In the present study, we demonstrate that sDAPAL is likely to follow anti-E2 mechanism of β-elimination of DAP, by mutational analysis of Thr385 which also results in broader substrate specificity. The Asp125 abstracts proton from D-DAP and Asp194 assists in substrate binding and stabilization. In the absence of intra-subunit disulfide bond, the activity of sDAPAL is stimulated by potassium ions.

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      Dose-dependent inhibitory effects of proton pump inhibitors on human osteoclastic and osteoblastic cell activity (pages 5052–5064)

      João Costa-Rodrigues, Sara Reis, Sónia Teixeira, Sandra Lopes and Maria H. Fernandes

      Version of Record online: 5 SEP 2013 | DOI: 10.1111/febs.12478

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      Human osteoclast precursors and mesenchymal stem cells were treated with the proton pump inhibitors (PPIs) omeprazole, esomeprazole and lansoprazole (10−7–10−3 m), for 21 days. PPIs caused a dose-dependent decrease in the differentiation and function of osteoclastic and osteoblastic cells, at concentrations ≥ 10−5 m. PPIs showed similar qualitative and quantitative effects, but displayed some differences in the underlying intracellular signaling pathways.

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      Role of N-terminal extension of Bacillus stearothermophilus RNase H2 and C-terminal extension of Thermotoga maritima RNase H2 (pages 5065–5079)

      Etin-Diah Permanasari, Clement Angkawidjaja, Yuichi Koga and Shigenori Kanaya

      Version of Record online: 5 SEP 2013 | DOI: 10.1111/febs.12479

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      The Bacillus stearothermophilus RNase H2 (BstRNH2) derivative without an N-terminal extension (BstRNH2ΔN) and Thermotoga maritima RNase H2 (TmaRNH2) derivative without a C-terminal extension (TmaRNH2ΔC) were constructed and their biochemical properties were compared with those of their intact partners. These extensions were shown to be important for activity, substrate-binding affinity, and stability of these enzymes.

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      Implications of enzyme deficiencies on mitochondrial energy metabolism and reactive oxygen species formation of neurons involved in rotenone-induced Parkinson's disease: a model-based analysis (pages 5080–5093)

      Nikolaus Berndt, Herrmann-Georg Holzhütter and Sascha Bulik

      Version of Record online: 12 SEP 2013 | DOI: 10.1111/febs.12480

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      Impaired mitochondrial energy metabolism and increased ROS production are hallmarks of neurodegenerative diseases. Kinetic modelling was applied to study mitochondrial metabolism in Parkinson's disease. Reduced activities of α-ketoglutarate-dehydrogenase and complex I contribute synergistically to energetic failure but antagonistically to ROS formation. Our model allows the evaluation of mitochondrial enzymes as potential targets for the pharmaceutical treatment of neurodegenerative diseases.

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      The metabolic modulator trimetazidine triggers autophagy and counteracts stress-induced atrophy in skeletal muscle myotubes (pages 5094–5108)

      Elisabetta Ferraro, Anna Maria Giammarioli, Sara Caldarola, Pasquale Lista, Alessandra Feraco, Antonella Tinari, Anna Maria Salvatore, Walter Malorni, Libera Berghella and Giuseppe Rosano

      Version of Record online: 12 SEP 2013 | DOI: 10.1111/febs.12484

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      Modulation of myotube metabolism by TMZ (Tz) triggers pathways which protect from atrophy. In particular, TMZ limits the reduction of myotube size induced by atrophic factors such as starvation (Stv), stimulates pathways reducing protein degradation (namely, the PI3K-Akt-mTORC2 pathway), increases MyHC expression and induces autophagy (as shown by LC3-II increase), a key mechanism involved in muscle mass regulation.

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      The epigenetically-regulated miR-663 targets H-ras in K-562 cells (pages 5109–5117)

      Yang Yang, Li-Li Wang, Heng-Xiang Wang, Zi-Kuan Guo, Xiao-Fang Gao, Jian Cen, Yong-Hui Li, Li-Ping Dou and Li Yu

      Version of Record online: 12 SEP 2013 | DOI: 10.1111/febs.12485

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      We report that the CpG islands in the upstream region of pre-miR-663 are aberrantly methylated in the k-562 cell line and in the white blood cells of some CML patients and that H-ras is one of the genes targeted by miR-663. Over-expression of miR-663 may suppress proliferation of the k-562 cell line in part by enhancing cell apoptosis.

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      Angiogenesis enhanced by Phyllocaulis boraceiensis mucus in human cells (pages 5118–5127)

      Ana R. de Toledo-Piza and Durvanei A. Maria

      Version of Record online: 12 SEP 2013 | DOI: 10.1111/febs.12487

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      Phyllocaulis boraceiensis mucus is known to be capable of inducing cell proliferation and enhancing the wound healing process. We demonstrate here that the angiogenesis process is also enhanced in endothelial cells and fibroblasts treated with P. boraceiensis mucus. VEGF-R1 and CD-34 expression was increased in endothelial cells cultivated with 0.012 μg·μL−1 P. boraceiensis mucus. This compound enhanced angiogenesis.

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      Cotton GhMPK6a negatively regulates osmotic tolerance and bacterial infection in transgenic Nicotiana benthamiana, and plays a pivotal role in development (pages 5128–5144)

      Yuzhen Li, Liang Zhang, Xiuling Wang, Wei Zhang, Lili Hao, Xiaoqian Chu and Xingqi Guo

      Version of Record online: 5 SEP 2013 | DOI: 10.1111/febs.12488

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      Cotton (Gossypium hirsutum) GhMPK6a is stress responsive and can negatively regulate osmotic tolerance and bacterial infection in transgenic Nicotiana benthamiana, and plays a pivotal role in development. GhMPK6a interacts with upstream MAPK kinase GhMKK4, as evidenced by yeast two-hybrid and bimolecular fluorescence complementation (BiFC) systems. These results broaden the information of MAPK cascades in cotton crops.

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      Phosphorylation of Noxo1 at threonine 341 regulates its interaction with Noxa1 and the superoxide-producing activity of Nox1 (pages 5145–5159)

      Asataro Yamamoto, Ryu Takeya, Masaki Matsumoto, Keiichi I. Nakayama and Hideki Sumimoto

      Version of Record online: 12 SEP 2013 | DOI: 10.1111/febs.12489

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      Superoxide production by the NAPDH oxidase Nox1, which requires expression of its regulatory proteins Noxo1 and Noxa1, is markedly enhanced upon cell stimulation with phorbol myristate acetate, a potent activator of protein kinase C (PKC). Here, we show that PKC directly phosphorylates Noxo1 at Thr341, and the phosphorylation facilitates Noxo1 interaction with Noxa1, thereby enhancing the superoxide-producing activity of Nox1.

  6. Author index

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Editorial
    5. Focus on Mitochondria Series
    6. Original Articles
    7. Author index
    8. Table of Contents
    1. You have free access to this content
      Author index (page 5160)

      Version of Record online: 1 OCT 2013 | DOI: 10.1111/j.1742-4658.2013.08797.x

  7. Table of Contents

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Editorial
    5. Focus on Mitochondria Series
    6. Original Articles
    7. Author index
    8. Table of Contents
    1. You have free access to this content
      Table of Contents (page 5161)

      Version of Record online: 1 OCT 2013 | DOI: 10.1111/febs.12540

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