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  • The composition of the gut microbiota shapes the colon mucus barrier
    1. Hedvig E Jakobsson1,
    2. Ana M Rodríguez‐Piñeiro1,
    3. André Schütte1,
    4. Anna Ermund1,
    5. Preben Boysen2,
    6. Mats Bemark3,4,
    7. Felix Sommer5,
    8. Fredrik Bäckhed5,
    9. Gunnar C Hansson1 and
    10. Malin EV Johansson*,1
    1. 1Department of Medical Biochemistry, University of Gothenburg, Gothenburg, Sweden
    2. 2Department of Food Safety and Infection Biology, Faculty of Veterinary Medicine and Biosciences Norwegian University of Life Sciences, Oslo, Norway
    3. 3Department of Microbiology and Immunology, University of Gothenburg, Gothenburg, Sweden
    4. 4Department of Clinical Immunology and Transfusion Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden
    5. 5The Wallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden
    1. *Corresponding author. Tel: +46 31 786 3487; E‐mail: malin.johansson{at}medkem.gu.se

    Mice of the same strain living in the same animal facility can have distinct microbiotas, which affects the penetrability of the colon mucus barrier in a transmissible manner. Free‐living mice have impenetrable mucus, as one of the experimental groups.

    Synopsis

    Mice of the same strain living in the same animal facility can have distinct microbiotas, which affects the penetrability of the colon mucus barrier in a transmissible manner. Free‐living mice have impenetrable mucus, as one of the experimental groups.

    • The colon microbiota influences the penetrability of the inner mucus layer.

    • Certain bacteria are associated with a more penetrable inner mucus layer.

    • The mucus phenotype was transmissible by transfer of the microbiota to germ‐free mice.

    • Bacteria
    • Colon
    • Intestine
    • MUC2
    • Mucus
    • Received July 3, 2014.
    • Revision received December 1, 2014.
    • Accepted December 2, 2014.

    This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs 4.0 License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

    Hedvig E Jakobsson, Ana M Rodríguez‐Piñeiro, André Schütte, Anna Ermund, Preben Boysen, Mats Bemark, Felix Sommer, Fredrik Bäckhed, Gunnar C Hansson, Malin EV Johansson
  • Living too longThe current focus of medical research on increasing the quantity, rather than the quality, of life is damaging our health and harming the economy

    The current focus of medical research on increasing the quantity, rather than the quality, of life is damaging our health and harming the economy

    1. Guy C Brown (gcb3{at}cam.ac.uk) 1
    1. 1Department of Biochemistry, University of Cambridge, Cambridge, UK

    Longer lifespans, often ending with multiple diseases, threaten the viability of social and health systems. Rather than prolonging life further, research and funding should focus on increasing the quality of life in old age.

    Guy C Brown
  • Stem and progenitor cell dysfunction in human trisomies
    1. Binbin Liu1,
    2. Sarah Filippi2,
    3. Anindita Roy3 and
    4. Irene Roberts*,1
    1. 1Department of Paediatrics and Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, Oxford, UK
    2. 2Department of Statistics, University of Oxford, Oxford, UK
    3. 3Centre for Haematology, Imperial College London, London, UK
    1. *Corresponding author. Tel: +44 1865 222316; Fax: +44 1865 234251; E‐mail: irene.roberts{at}paediatrics.ox.ac.uk

    This review analyzes the impact of human trisomies on stem and progenitor cell functions with a special focus on trisomy 21 and hematopoiesis.

    • Down syndrome
    • hematopoietic stem cells
    • leukemia
    • neural progenitors
    • trisomy 21
    • Received September 14, 2014.
    • Revision received November 16, 2014.
    • Accepted November 20, 2014.
    Binbin Liu, Sarah Filippi, Anindita Roy, Irene Roberts
  • Vesicle uncoating regulated by SH3‐SH3 domain‐mediated complex formation between endophilin and intersectin at synapses
    1. Arndt Pechstein1,2,,
    2. Fabian Gerth3,,
    3. Ira Milosevic4,
    4. Maria Jäpel1,
    5. Marielle Eichhorn‐Grünig1,
    6. Olga Vorontsova2,
    7. Jelena Bacetic1,
    8. Tanja Maritzen1,
    9. Oleg Shupliakov*,2,
    10. Christian Freund*,3 and
    11. Volker Haucke*,1
    1. 1Leibniz‐Institut für Molekulare Pharmakologie (FMP), Berlin, Germany
    2. 2Department of Neuroscience, DBRM, Karolinska Institutet, Stockholm, Sweden
    3. 3Institute of Chemistry and Biochemistry, Freie Universität Berlin, Berlin, Germany
    4. 4European Neuroscience Institute Göttingen (ENI‐G), Synaptic Vesicle Dynamics Group, Göttingen, Germany
    1. * Corresponding author. Tel: +46 852487849; E‐mail: oleg.shupliakov{at}ki.se

      Corresponding author. Tel: +49 30 83851187; E‐mail: christian.freund{at}fu-berlin.de

      Corresponding author. Tel: +49 30 94793101; E‐mail: haucke{at}fmp-berlin.de

    1. Equal contributions

    Neurotransmission requires endocytic membrane retrieval and clathrin‐mediated reformation of synaptic vesicles. This study shows that intersectin 1 directly associates with the BAR domain protein endophilin to facilitate vesicle uncoating at synapses.

    Synopsis

    Neurotransmission requires endocytic membrane retrieval and clathrin‐mediated reformation of synaptic vesicles. This study shows that intersectin 1 directly associates with the BAR domain protein endophilin to facilitate vesicle uncoating at synapses.

    • Intersectin 1 knockout mice accumulate clathrin‐coated vesicles akin to endophilin A loss.

    • Intersectin via its SH3B domain directly binds to endophilin A.

    • Intersectin binding is required for endophilin function in vesicle uncoating.

    • endophilin
    • intersectin
    • neurotransmission
    • SH3 domains
    • synaptic vesicle recycling
    • Received July 2, 2014.
    • Revision received November 28, 2014.
    • Accepted December 1, 2014.

    This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs 4.0 License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

    Arndt Pechstein, Fabian Gerth, Ira Milosevic, Maria Jäpel, Marielle Eichhorn‐Grünig, Olga Vorontsova, Jelena Bacetic, Tanja Maritzen, Oleg Shupliakov, Christian Freund, Volker Haucke
  • Lessons in learningAn effective process for engaging 12‐ to 14‐year‐olds in stem cell biology

    An effective process for engaging 12‐ to 14‐year‐olds in stem cell biology

    1. Emma Kemp (enquiries{at}eurostemcell.org) 1 and
    2. Ian Chambers (ichambers{at}ed.ac.uk) 1,2
    1. 1MRC Centre for Regenerative Medicine University of Edinburgh, Edinburgh, UK
    2. 2Institute for Stem Cell Research School of Biological Sciences University of Edinburgh, Edinburgh, UK

    Engaging school children with cutting‐edge science remains challenging. Here, the authors reflect on their experience of developing lessons for high school children about the scientific, medical and ethical implications of stem cell research.

    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.

    Emma Kemp, Ian Chambers
  • Hop/Sti1 phosphorylation inhibits its co‐chaperone function
    1. Alina Röhl1,
    2. Franziska Tippel1,
    3. Evelyn Bender1,
    4. Andreas B Schmid1,
    5. Klaus Richter1,
    6. Tobias Madl1,2,3 and
    7. Johannes Buchner*,1
    1. 1Center for Integrated Protein Science (CIPSM) at the Department Chemie, Technische Universität München, Garching, Germany
    2. 2Institute of Structural Biology Helmholtz Zentrum München, Neuherberg, Germany
    3. 3Institute of Molecular Biology & Biochemistry, Center of Molecular Medicine, Medical University of Graz, Graz, Austria
    1. *Corresponding author. Tel: +49 89 28913340; E‐mail: johannes.buchner{at}tum.de

    This study shows that Hop and Sti1 are phosphorylated, and the sites and magnitude of the effects are species specific, with Hop being more tightly regulated. Phosphorylation negatively affects interaction with Hsp70.

    Synopsis

    This study shows that Hop and Sti1 are phosphorylated, and the sites and magnitude of the effects are species specific, with Hop being more tightly regulated. Phosphorylation negatively affects interaction with Hsp70.

    • Yeast Sti1 and human Hop share highly conserved functions.

    • Human Hsp90 is not inhibited to the same degree as yeast Hsp90 by Sti1/Hop.

    • Phosphorylation of Hop at a unique position affects its structure.

    • Phosphorylation of Sti1/Hop negatively affects client maturation.

    • co‐chaperone
    • phosphorylation
    • regulation
    • SAXS
    • Sti1/Hop
    • Received June 20, 2014.
    • Revision received November 18, 2014.
    • Accepted November 20, 2014.

    This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs 4.0 License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

    Alina Röhl, Franziska Tippel, Evelyn Bender, Andreas B Schmid, Klaus Richter, Tobias Madl, Johannes Buchner
  • Functional analysis of related CrRLK1L receptor‐like kinases in pollen tube reception
    1. Sharon A Kessler*,1,2,
    2. Heike Lindner1,
    3. Daniel S Jones2 and
    4. Ueli Grossniklaus*,1
    1. 1Institute of Plant Biology & Zürich‐Basel Plant Science Center, University of Zürich, Zürich, Switzerland
    2. 2Department of Microbiology and Plant Biology, University of Oklahoma, Norman, OK, USA
    1. * Corresponding author. Tel: +1 405 325 5085; E‐mail: sakessler{at}ou.edu

      Corresponding author. Tel: +41 44 634 82 40; E‐mail: grossnik{at}botinst.uzh.ch

    Plant CrRLK1L receptor‐like kinases are involved in various signaling processes. Domain swapping shows that, for pollen tube reception, the extracellular domains of three members (FER, ANX1, HERK1) are not interchangeable, whereas their intercellular domains are functionally equivalent.

    Synopsis

    Plant CrRLK1L receptor‐like kinases are involved in various signaling processes. Domain swapping shows that, for pollen tube reception, the extracellular domains of three members (FER, ANX1, HERK1) are not interchangeable, whereas their intercellular domains are functionally equivalent.

    • Extracellular domains of the FER, ANX1 and HERK1 receptor‐like kinases are not interchangeable for their function in pollen tube reception, but their intracellular domains are.

    • Kinase‐dead FER protein can complement the fer mutant.

    • Arabidopsis
    • FERONIA
    • pollen tube reception
    • receptor‐like kinases
    • signaling
    • Received April 2, 2014.
    • Revision received November 10, 2014.
    • Accepted November 11, 2014.
    Sharon A Kessler, Heike Lindner, Daniel S Jones, Ueli Grossniklaus