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  • Plasma membrane H+‐ATPase regulation is required for auxin gradient formation preceding phototropic growth
    1. Tim Hohm1,2,,
    2. Emilie Demarsy3,,
    3. Clément Quan3,
    4. Laure Allenbach Petrolati3,
    5. Tobias Preuten3,
    6. Teva Vernoux4,
    7. Sven Bergmann*,1,2, and
    8. Christian Fankhauser*,3,
    1. 1Department of Medical Genetics, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland
    2. 2Swiss Institute for Bioinformatics, Lausanne, Switzerland
    3. 3Centre for Integrative Genomics, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland
    4. 4Laboratoire de Reproduction et Développement des Plantes, CNRS INRA ENS Lyon UCBL Université de Lyon, Lyon, France
    1. * Corresponding author. Tel: +41 21 692 5452; E‐mail: sven.bergmann{at}unil.ch

      Corresponding author. Tel: +41 21 692 3941; E‐mail: christian.fankhauser{at}unil.ch

    1. These authors contributed equally to this work

    2. These authors contributed equally to this work

    In silico and in planta analyses of the contribution of morphological and biophysical parameters to auxin relocalization in phototropism reveal the importance of light‐dependent regulation of apoplastic pH and of cellular topology.

    Synopsis

    In silico and in planta analyses of the contribution of morphological and biophysical parameters to auxin relocalization in phototropism reveal the importance of light‐dependent regulation of apoplastic pH and of cellular topology.

    • Regulation of apoplastic pH is a key feature for the establishment of a lateral auxin gradient leading to phototropism.

    • The phototropin photoreceptors regulate the activity of plasma membrane‐associated H+‐ATPase which are major regulators of apoplastic pH.

    • Cellular topology has a strong impact on lateral auxin gradient formation.

    • auxin
    • modeling
    • phototropins
    • phototropism
    • plasma membrane H+‐ATPase

    Mol Syst Biol. (2014) 10: 751

    • Received March 2, 2014.
    • Revision received August 20, 2014.
    • Accepted August 22, 2014.

    This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

    Tim Hohm, Emilie Demarsy, Clément Quan, Laure Allenbach Petrolati, Tobias Preuten, Teva Vernoux, Sven Bergmann, Christian Fankhauser
  • The role of the interactome in the maintenance of deleterious variability in human populations
    1. Luz Garcia‐Alonso1,
    2. Jorge Jiménez‐Almazán1,2,
    3. Jose Carbonell‐Caballero1,
    4. Alicia Vela‐Boza3,
    5. Javier Santoyo‐López3,
    6. Guillermo Antiñolo3,4,5 and
    7. Joaquin Dopazo*,1,2,3,6
    1. 1Computational Genomics Department, Centro de Investigación Príncipe Felipe (CIPF), Valencia, Spain
    2. 2Bioinformatics of Rare Diseases (BIER), CIBER de Enfermedades Raras (CIBERER), Valencia, Spain
    3. 3Medical Genome Project, Genomics and Bioinformatics Platform of Andalusia (GBPA), Seville, Spain
    4. 4Department of Genetics, Reproduction and Fetal Medicine, Institute of Biomedicine of Seville, University Hospital Virgen del Rocio/Consejo Superior de Investigaciones Científicas/University of Seville, Seville, Spain
    5. 5Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Seville, Spain
    6. 6Functional Genomics Node, (INB) at CIPF, Valencia, Spain
    1. *Corresponding author. Tel: +34 96 328 9680; E‐mail: jdopazo{at}cipf.es

    Analysis of genetic variability in 1,330 personal genomes obtained by exome sequencing of healthy individuals indicates that deleterious mutations preferentially accumulate in the periphery of the interactome and occur in specific combinations that minimally disrupt its structure.

    Synopsis

    Analysis of genetic variability in 1,330 personal genomes obtained by exome sequencing of healthy individuals indicates that deleterious mutations preferentially accumulate in the periphery of the interactome and occur in specific combinations that minimally disrupt its structure.

    • The large mutational load of human genome was analyzed in the context of the protein interactome.

    • Deleterious mutations tolerated by healthy individuals are found to accumulate in the periphery of the interactome.

    • Such mutations only occur in specific epistatic combinations that minimize the impact over the interactome.

    • The study suggests that the pathological potential of a variant seems to be more a systems property than an intrinsic property of individual proteins.

    • exome sequencing
    • interactome
    • mutational load
    • network analysis
    • robustness

    Mol Syst Biol. (2014) 10: 752

    • Received February 22, 2014.
    • Revision received August 23, 2014.
    • Accepted August 28, 2014.

    This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

    Luz Garcia‐Alonso, Jorge Jiménez‐Almazán, Jose Carbonell‐Caballero, Alicia Vela‐Boza, Javier Santoyo‐López, Guillermo Antiñolo, Joaquin Dopazo
  • Apoptosis and other immune biomarkers predict influenza vaccine responsiveness
    David Furman, Vladimir Jojic, Brian Kidd, Shai Shen‐Orr, Jordan Price, Justin Jarrell, Tiffany Tse, Huang Huang, Peder Lund, Holden T Maecker, Paul J Utz, Cornelia L Dekker, Daphne Koller, Mark M Davis
  • Systematic analysis of somatic mutations in phosphorylation signaling predicts novel cancer drivers
    Jüri Reimand, Gary D Bader
  • Quantitative analysis of mammalian translation initiation sites by FACS‐seq
    1. William L Noderer1,
    2. Ross J Flockhart2,
    3. Aparna Bhaduri2,3,
    4. Alexander J Diaz de Arce1,
    5. Jiajing Zhang2,
    6. Paul A Khavari2,4 and
    7. Clifford L Wang*,1
    1. 1Department of Chemical Engineering, Stanford University, Stanford, CA, USA
    2. 2The Program in Epithelial Biology, Stanford University School of Medicine, Stanford, CA, USA
    3. 3The Program in Cancer Biology, Stanford University School of Medicine, Stanford, CA, USA
    4. 4Veterans Affairs Palo Alto Healthcare System, Palo Alto, CA, USA
    1. *Corresponding author. Tel: +1 650 736 1807; Fax: +1 650 725 7294; E‐mail: cliff.wang{at}stanford.edu

    The impact of the translation initiation site (TIS) sequence on translational efficiency is determined by FACS‐seq, combining cell sorting and high‐throughput sequencing. A quantitative model of initiation links TIS mutations with tumorigenesis and predicts translational protein isoforms.

    Synopsis

    The impact of the translation initiation site (TIS) sequence on translational efficiency is determined by FACS‐seq, combining cell sorting and high‐throughput sequencing. A quantitative model of initiation links TIS mutations with tumorigenesis and predicts translational protein isoforms.

    • Translation efficiency is analyzed for all possible TIS sequences utilizing an AUG start codon and an RYMRMVAUGGC motif is found to be optimal for translation initiation.

    • Dinucleotide interactions, which cannot be conveyed in a single motif, influence initiation efficiency.

    • TIS mutations affect protein expression similarly to known tumor expression patterns, thereby putatively linking the mutations and tumor formation.

    • Leaky scanning results in N‐terminal truncated protein isoforms and enhances proteome diversity.

    • FACS‐seq
    • Kozak motif
    • proteome modeling
    • start codon
    • translation initiation

    Mol Syst Biol. (2014) 10: 748

    • Received January 17, 2014.
    • Revision received July 22, 2014.
    • Accepted July 24, 2014.

    This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

    William L Noderer, Ross J Flockhart, Aparna Bhaduri, Alexander J Diaz de Arce, Jiajing Zhang, Paul A Khavari, Clifford L Wang
  • Emergence of robust growth laws from optimal regulation of ribosome synthesis
    1. Matthew Scott*,1,
    2. Stefan Klumpp2,
    3. Eduard M Mateescu3 and
    4. Terence Hwa3,4
    1. 1Department of Applied Mathematics, University of Waterloo, Waterloo, ON, Canada
    2. 2Max Planck Institute of Colloids and Interfaces, Potsdam, Germany
    3. 3Department of Physics and Center for Theoretical Biological Physics, University of California, San Diego La Jolla, CA, USA
    4. 4Institute for Theoretical Studies, ETH Zurich, Zurich, Switzerland
    1. *Corresponding author. Tel: +1 519 888 4567 ext. 35454; E‐mail: mscott{at}math.uwaterloo.ca

    Building upon empirical “growth laws”, this Perspective discusses mechanisms that integrate protein synthesis with amino acid flux and metabolic control to guarantee optimal growth irrespective of the nutrient environment.

    • growth control
    • metabolic control
    • phenomenological model
    • resource allocation
    • synthetic biology

    Mol Syst Biol. (2014) 10: 747

    • Received April 20, 2014.
    • Revision received July 11, 2014.
    • Accepted July 14, 2014.

    This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

    Matthew Scott, Stefan Klumpp, Eduard M Mateescu, Terence Hwa
  • Specificity, propagation, and memory of pericentric heterochromatin
    1. Katharina Müller‐Ott1,
    2. Fabian Erdel1,
    3. Anna Matveeva2,
    4. Jan‐Philipp Mallm1,
    5. Anne Rademacher1,
    6. Matthias Hahn3,
    7. Caroline Bauer1,
    8. Qin Zhang2,
    9. Sabine Kaltofen14,
    10. Gunnar Schotta3,
    11. Thomas Höfer2 and
    12. Karsten Rippe*,1
    1. 1Deutsches Krebsforschungszentrum (DKFZ) and BioQuant, Research Group Genome Organization & Function, Heidelberg, Germany
    2. 2Deutsches Krebsforschungszentrum (DKFZ) and BioQuant, Division Theoretical Systems Biology, Heidelberg, Germany
    3. 3Munich Center for Integrated Protein Science and Adolf Butenandt Institute, Ludwig Maximilians University, Munich, Germany
    4. 4 Biochemistry & Structural Biology, Lund University, Lund, Sweden
    1. *Corresponding author. Tel: +49 6221 5451376; Fax: +49 6221 5451487; E‐mail: karsten.rippe{at}dkfz.de

    A comprehensive analysis of the epigenetic network that silences pericentric heterochromatin (PCH) transcription in mouse fibroblasts is presented. The resulting quantitative model explains the spatial extension, stability and propagation of histone modification domains.

    Synopsis

    A comprehensive analysis of the epigenetic network that silences pericentric heterochromatin (PCH) transcription in mouse fibroblasts is presented. The resulting quantitative model explains the spatial extension, stability and propagation of histone modification domains.

    • A quantitative map of the abundance and interactions of 16 PCH factors is generated by fluorescence microscopy/spectroscopy and ChIP‐seq.

    • A predictive mathematical model, based on the quantitative data, explains how the silenced PCH state is maintained and transmitted through the cell cycle.

    • A “nucleation and looping” mechanism is proposed, in which chromatin‐bound SUV39H1/2 complexes act as nucleation sites and propagate a spatially confined PCH domain with elevated H3K9me3 modifications via chromatin dynamics.

    • FRAP/FCS
    • heterochromatin protein 1
    • histone methylation
    • pericentric heterochromatin
    • protein network

    Mol Syst Biol. (2014) 10: 746

    • Received April 19, 2014.
    • Revision received July 10, 2014.
    • Accepted July 15, 2014.

    This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

    Katharina Müller‐Ott, Fabian Erdel, Anna Matveeva, Jan‐Philipp Mallm, Anne Rademacher, Matthias Hahn, Caroline Bauer, Qin Zhang, Sabine Kaltofen, Gunnar Schotta, Thomas Höfer, Karsten Rippe

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