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Development & Differentiation

  • Open Access
    MYC proteins promote neuronal differentiation by controlling the mode of progenitor cell division
    MYC proteins promote neuronal differentiation by controlling the mode of progenitor cell division
    1. Nikolay Zinin1,†,
    2. Igor Adameyko2,†,
    3. Margareta Wilhelm1,
    4. Nicolas Fritz2,
    5. Per Uhlén2,
    6. Patrik Ernfors2 and
    7. Marie Arsenian Henriksson*,1
    1. 1Department of Microbiology, Tumor and Cell Biology (MTC) Karolinska Institutet, Stockholm, Sweden
    2. 2Department of Medical Biochemistry and Biophysics (MBB), Karolinska Institutet, Stockholm, Sweden
    1. ↵*Corresponding author: Tel: +46 8 524 86205; Fax: +46 8 330744; E‐mail: marie.henriksson{at}ki.se.
    1. ↵† These authors contributed equally.

    This study reveals an unexpected role for MYC in the control of stemness versus differentiation of neural stem cells in vivo and shows that Myc represses Notch signaling and promotes asymmetric neurogenic cell divisions.

    Synopsis

    This study reveals an unexpected role for MYC in the control of stemness versus differentiation of neural stem cells in vivo and shows that Myc represses Notch signaling and promotes asymmetric neurogenic cell divisions.

    • Elevated MYC levels increase neurogenesis in the developing chick neural tube

    • The neurogenic function of MYC depends on the integrity of the polarized neural tissue

    • MYC promotes apico‐basal neurogenic divisions

    • Asymmetric division
    • differentiation
    • MYC
    • neural progenitor
    • Notch
    • Received April 19, 2013.
    • Revision received December 9, 2013.
    • Accepted December 15, 2013.
    • © 2014 The Authors. Published under the terms of the CC BY NC ND license.

    This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs 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.

    Nikolay Zinin, Igor Adameyko, Margareta Wilhelm, Nicolas Fritz, Per Uhlén, Patrik Ernfors, Marie Arsenian Henriksson
    Published online 01.04.2014
    • Development & Differentiation
    • Neuroscience
  • You have access
    Dedifferentiation and reprogramming: origins of cancer stem cells
    Dedifferentiation and reprogramming: origins of cancer stem cells
    1. Dinorah Friedmann‐Morvinski1 and
    2. Inder M Verma*,1
    1. 1Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA, USA
    1. ↵*Corresponding author. Tel: +1 858 453 4100 x1462; Fax: +1 858 558 7454; E‐mail: verma{at}salk.edu

    Research in the reprogramming of somatic cells has also led to a better understanding of the origin of cancer stem cells. This review discusses cancers that may be the product of somatic cell reprogramming and as such constitute potential risks to the application of iPSCs in regenerative medicine.

    • cancer stem cells
    • dedifferentiation
    • somatic reprogramming
    • tumor plasticity

    EMBO Reports (2014) 15, 244–253

    • Received November 21, 2013.
    • Revision received January 14, 2014.
    • Accepted January 21, 2014.
    • © 2014 The Authors
    Dinorah Friedmann‐Morvinski, Inder M Verma
    Published online 01.03.2014
    • Cancer
    • Development & Differentiation
  • You have access
    Ars Moriendi; the art of dying well – new insights into the molecular pathways of necroptotic cell death
    Ars Moriendi; the art of dying well – new insights into the molecular pathways of necroptotic cell death
    1. James M Murphy*,1,2 and
    2. John Silke*,1,2
    1. 1The Walter and Eliza Hall Institute of Medical Research, Parkville, Vic., Australia
    2. 2Department of Medical Biology, University of Melbourne, Parkville, Vic., Australia
    1. ↵* Corresponding author. Tel: +61 3 93452945; Fax: +61 393470852; E‐mail: j.silke{at}latrobe.edu.au
      Corresponding author. Tel: +61 3 93452407; Fax: +61 393470852; E‐mail: jamesm{at}wehi.edu.au

    John Silke and James Murphy review current advances in our understanding of the events that lead to programmed necrosis from a structural perspective. They place these insights in a biological context by discussing relevant studies with knock‐out animals.

    • necroptosis
    • RIP kinases
    • MLKL
    • cIAP
    • TNF

    EMBO Reports (2014) 15, 155–164

    • Received September 10, 2013.
    • Revision received December 6, 2013.
    • Accepted December 10, 2013.
    • © 2014 The Authors
    James M Murphy, John Silke
    Published online 01.02.2014
    • Development & Differentiation
  • You have access
    The SCFSlimb E3 ligase complex regulates asymmetric division to inhibit neuroblast overgrowth
    The SCF<sup>Slimb</sup> E3 ligase complex regulates asymmetric division to inhibit neuroblast overgrowth
    1. Song Li1,2,
    2. Cheng Wang1,
    3. Edwin Sandanaraj3,4,
    4. Sherry S Y Aw18,
    5. Chwee T Koe1,2,
    6. Jack J L Wong2,5,
    7. Fengwei Yu1,2,5,
    8. Beng T Ang3,4,6,
    9. Carol Tang4,6,7 and
    10. Hongyan Wang*,1,2,6
    1. 1Neuroscience & Behavioral Disorders Program, Duke‐National University of Singapore Graduate Medical School Singapore, Singapore City, Singapore
    2. 2NUS Graduate School for Integrative Sciences and Engineering National University of Singapore, Singapore City, Singapore
    3. 3Singapore Institute for Clinical Sciences A*STAR, Singapore City, Singapore
    4. 4National Neuroscience Institute, Singapore City, Singapore
    5. 5Temasek Life Sciences Laboratory and Department of Biological Sciences, National University of Singapore, Singapore City, Singapore
    6. 6Department of Physiology, Yong Loo Lin School of Medicine National University of Singapore, Singapore City, Singapore
    7. 7Division of Medical Sciences, Humphrey Oei Institute of Cancer Research National Cancer Centre, Singapore City, Singapore
    8. 8Institute of Molecular and Cell Biology, Singapore City, Singapore
    1. ↵*Corresponding author. Tel: +65 6516 7740; Fax: +65 6557 0729; E‐mail: hongyan.wang{at}duke-nus.edu.sg

    This report provides evidence that loss of the SCFSlimb E3 ubiquitin ligase complex as well as hyperactivation of Akt lead to neuroblast overgrowth and defects in asymmetric cell division. Slimb, the F‐box protein of the SCF complex, associates with Akt in a protein complex, and SCFSlimb acts through SAK and Akt to inhibit neuroblast overgrowth.

    Synopsis

    This report provides evidence that loss of the SCFSlimb E3 ubiquitin ligase complex as well as hyperactivation of Akt lead to neuroblast overgrowth and defects in asymmetric cell division. Slimb, the F‐box protein of the SCF complex, associates with Akt in a protein complex, and SCFSlimb acts through SAK and Akt to inhibit neuroblast overgrowth.

    • The SCFSlimb E3 ubiquitin ligase inhibits neuroblast (NB) overgrowth and regulates asymmetric division of NBs.

    • The NB overgrowth phenotype in the absence of SCFSlimb is similar to what is seen in conditions of AKT hyperactivation.

    • The F‐box protein Slimb associates with AKT and regulates NB overgrowth via SAK and AKT.

    • asymmetric division
    • neuroblasts
    • polarity
    • the SCF complex

    EMBO Reports (2014) 15, 165–174

    • Received September 9, 2013.
    • Revision received November 18, 2013.
    • Accepted November 19, 2013.
    • © 2014 The Authors
    Song Li, Cheng Wang, Edwin Sandanaraj, Sherry S Y Aw, Chwee T Koe, Jack J L Wong, Fengwei Yu, Beng T Ang, Carol Tang, Hongyan Wang
    Published online 01.02.2014
    • Cell Adhesion, Polarity & Cytoskeleton
    • Development & Differentiation
  • Open Access
    Msd1/SSX2IP‐dependent microtubule anchorage ensures spindle orientation and primary cilia formation
    Msd1/SSX2IP‐dependent microtubule anchorage ensures spindle orientation and primary cilia formation
    1. Akiko Hori1,
    2. Chiho Ikebe13,
    3. Masazumi Tada2 and
    4. Takashi Toda*,1
    1. 1Laboratory of Cell Regulation UK, London Research Institute, London, UK
    2. 2Department of Cell and Developmental Biology, University College London, London, UK
    3. 3William Harvey Research Institute Barts and The London Queen Mary's School of Medicine and Dentistry, London, UK
    1. ↵*Corresponding author. Tel: +44 20 7269 3535; Fax: +44 20 7269 3258; E‐mail: toda{at}cancer.org.uk

    The human protein Msd1/SSX2IP is identified as a microtubule‐anchoring factor at the centrosome and is essential for primary cilia formation. The zebrafish orthologue is also required for cilia formation and determines left‐right asymmetry.

    Synopsis

    The human protein Msd1/SSX2IP is identified as a microtubule‐anchoring factor at the centrosome and is essential for primary cilia formation. The zebrafish orthologue is also required for cilia formation and determines left‐right asymmetry.

    • Human Msd1/SSX2IP protein is a conserved microtubule‐anchoring factor at the centrosome.

    • Human and zebrafish Msd1 are essential for primary cilia formation.

    • Zebrafish Msd1 determines left‐right asymmetry during embryogenesis.

    • centrosome
    • ciliogenesis
    • left‐right symmetry
    • microtubule anchoring
    • spindle orientation

    EMBO Reports (2014) 15, 175–184

    • Received August 29, 2013.
    • Revision received November 5, 2013.
    • Accepted November 8, 2013.
    • © 2014 The Authors.

    This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs 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.

    Akiko Hori, Chiho Ikebe, Masazumi Tada, Takashi Toda
    Published online 01.02.2014
    • Cell Cycle
    • Development & Differentiation
  • You have access
    Cellular dynamics in the muscle satellite cell niche
    1. C Florian Bentzinger1,
    2. Yu Xin Wang1,2,
    3. Nicolas A Dumont1 and
    4. Michael A Rudnicki*,1,2
    1. 1 Sprott Center for Stem Cell Research, Ottawa Hospital Research Institute, 501 Smyth Road, Ottawa, Ontario, K1H 8L6, Canada
    2. 2 Faculty of Medicine, Department of Cellular and Molecular Medicine, University of Ottawa, 451 Smyth Road, Ottawa, Ontario, K1H 8M5, Canada
    1. ↵*Corresponding author. Tel: 00 1 (613) 739 6740; Fax: 00 1 (613) 739 6294; E-mail: mrudnicki{at}ohri.ca

    Multiple, functionally diverse cell types have been shown to contribute to skeletal muscle regeneration. This Review discusses the cellular dynamics and the roles of immune, fibrogenic, vessel‐associated and myogenic cells in the response of the satellite cell niche to muscle injury and disease.

    • skeletal muscle satellite cells
    • muscle stem cell niche
    • accessory cell types
    • myogenic cell types
    • muscular dystrophy
    • Received September 5, 2013.
    • Accepted October 21, 2013.
    • Copyright © 2013 European Molecular Biology Organization
    C Florian Bentzinger, Yu Xin Wang, Nicolas A Dumont, Michael A Rudnicki
    Published online 01.12.2013
    • Development & Differentiation
    • Molecular Biology of Disease
  • You have access
    Tightly controlled WRKY23 expression mediates Arabidopsis embryo development
    1. Wim Grunewald*,1,2,†,
    2. Ive De Smet*,1,2,3,†,
    3. Bert De Rybel4,
    4. Helene S Robert1,2,
    5. Brigitte van de Cotte1,2,
    6. Viola Willemsen5,
    7. Godelieve Gheysen6,
    8. Dolf Weijers4,
    9. Jiří Friml1,2 and
    10. Tom Beeckman1,2
    1. 1 Department of Plant Systems Biology, VIB, and Bioinformatics, Ghent University, 9052, Ghent, Belgium
    2. 2 Department of Plant Biotechnology and Bioinformatics, Ghent University, 9052, Ghent, Belgium
    3. 3 Plant and Crop Sciences Division, School of Biosciences, University of Nottingham, LE12 5RD, Loughborough, UK
    4. 4 Laboratory of Biochemistry, Wageningen University, 6703 HA, Wageningen, The Netherlands
    5. 5 Plant Developmental Biology Wageningen University, 6700 AP, Wageningen, The Netherlands
    6. 6 Department Molecular Biotechnology, Faculty of Bioscience Engineering, Ghent University, 9000, Ghent, Belgium
    1. ↵*Corresponding authors. Tel:+32 92446611; Fax:+32 92446610; E-mail: wim.grunewald{at}vib.be or Tel:+32 93313890; Fax:+32 93313809; E-mail: ive.desmet{at}psb.vib-ugent.be
    1. ↵† These authors contributed equally to this work.

    This study presents evidence that the tightly controlled expression of the transcription factor WRKY23 regulates both auxin‐dependent and auxin‐independent signalling pathways leading to root stem cell niche specification in Arabidopsis.

    • Arabidopsis
    • embryogenesis
    • WRKY
    • Received March 21, 2013.
    • Revision received October 4, 2013.
    • Accepted October 4, 2013.
    • Copyright © 2013 European Molecular Biology Organization
    Wim Grunewald, Ive De Smet, Bert De Rybel, Helene S Robert, Brigitte van de Cotte, Viola Willemsen, Godelieve Gheysen, Dolf Weijers, Jiří Friml, Tom Beeckman
    Published online 01.12.2013
    • Development & Differentiation
    • Plant Biology
    • Signal Transduction
  • Open Access
    Autophagy in Myf5+ progenitors regulates energy and glucose homeostasis through control of brown fat and skeletal muscle development
    1. Nuria Martinez‐Lopez1,2,†,
    2. Diana Athonvarangkul1,2,†,
    3. Srabani Sahu1,2,
    4. Luisa Coletto3,
    5. Haihong Zong1,4,
    6. Claire C Bastie1,4,5,
    7. Jeffrey E Pessin1,2,4,
    8. Gary J Schwartz1,4,6 and
    9. Rajat Singh*,1,2,4,7
    1. 1 Department of Medicine, Albert Einstein College of Medicine, Bronx, New York, 10461, USA
    2. 2 Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York, 10461, USA
    3. 3 Venetian Institute of Molecular Medicine, 35129, Padova, Italy
    4. 4 Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York, 10461, USA
    5. 5 Division of Metabolic and Vascular Health, Warwick Medical School, Coventry, CV4 7AL, UK
    6. 6 Department of Neuroscience, Albert Einstein College of Medicine, New York, 10461, USA
    7. 7 Institute for Aging Studies, Albert Einstein College of Medicine, New York, 10461, USA
    1. ↵*Corresponding author. Tel:+1 718 430 4118; Fax:+1 718 430 8557; E-mail: rajat.singh{at}einstein.yu.edu
    1. ↵† These authors contributed equally to this work.

    Atg7 deletion in Myf5+ progenitors blocks autophagy in brown adipose tissue and muscle, affecting their differentiation and function. Knockout mice have higher body temperatures and glucose intolerance, underscoring the importance of autophagy in these processes.

    • Autophagy
    • Myf5+ progenitors
    • brown fat
    • Received May 22, 2013.
    • Revision received June 26, 2013.
    • Accepted June 28, 2013.
    • Copyright © 2013 European Molecular Biology Organization

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

    Nuria Martinez‐Lopez, Diana Athonvarangkul, Srabani Sahu, Luisa Coletto, Haihong Zong, Claire C Bastie, Jeffrey E Pessin, Gary J Schwartz, Rajat Singh
    Published online 01.09.2013
    • Development & Differentiation
    • Metabolism
  • You have access
    Endless paces of degeneration—applying comparative genomics to study evolution's moulding of longevity
    1. João Pedro de Magalhães1 and
    2. Michael Kean1
    1. 1 Integrative Genomics of Ageing Group, Institute of Integrative Biology, University of Liverpool, Liverpool, UK

    Why do mice and humans have such different lifespans? Genome sequencing efforts are allowing researchers to pick apart the genetic foundations of longevity, with some promising results beginning to emerge.

    • Copyright © 2013 European Molecular Biology Organization
    João Pedro de Magalhães, Michael Kean
    Published online 01.08.2013
    • Development & Differentiation
    • Metabolism
    • Systems & Computational Biology
  • You have access
    Wnk kinases are positive regulators of canonical Wnt/β‐catenin signalling
    1. Ekatherina Serysheva1,2,
    2. Hebist Berhane3,4,
    3. Luca Grumolato5,6,
    4. Kubilay Demir7,
    5. Sophie Balmer1,2,
    6. Maxime Bodak3,4,
    7. Michael Boutros7,
    8. Stuart Aaronson5,
    9. Marek Mlodzik*,1,2 and
    10. Andreas Jenny*,3,4
    1. 1 Department of Developmental and Regenerative Biology, New York, New York, 10029, USA
    2. 2 Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, 10029, USA
    3. 3 Department of Developmental and Molecular Biology, Bronx, New York, USA
    4. 4 Department of Genetics, Albert Einstein College of Medicine, Bronx, New York, USA
    5. 5 Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York 10461, USA
    6. 6 INSERM U982‐University of Rouen, 76821, Mont Saint Aignan, France
    7. 7 German Cancer Research Center (DKFZ), Division of Signaling and Functional Genomics, and Heidelberg University, Medical Faculty Mannheim, Department for Cell and Molecular Biology, Im Neuenheimer Feld 580, Heidelberg 69120, Germany
    1. ↵*Corresponding authors. Tel:+1 212 241 6516; Fax:+1 212 241 8610; E-mail: marek.mlodzi{at}mssm.edu or Tel:+1 718 430 4183; Fax:+1 718 430 8567; E-mail: andreas.jenny{at}einstein.yu.edu

    This study identifies a novel role for Wnk kinases in canonical Wnt signalling that appears to be conserved from Drosophila to humans.

    • Dishevelled
    • Drosophila
    • Gordon syndrome
    • Wnk kinase
    • Wnt signalling
    • Received November 30, 2012.
    • Revision received May 29, 2013.
    • Accepted May 31, 2013.
    • Copyright © 2013 European Molecular Biology Organization
    Ekatherina Serysheva, Hebist Berhane, Luca Grumolato, Kubilay Demir, Sophie Balmer, Maxime Bodak, Michael Boutros, Stuart Aaronson, Marek Mlodzik, Andreas Jenny
    Published online 01.08.2013
    • Development & Differentiation

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Subject areas

  • Ageing (16)
  • Cancer (144)
  • Cell Adhesion, Polarity & Cytoskeleton (158)
  • Cell Cycle (195)
  • Autophagy & Cell Death (193)
  • Chemical Biology (10)
  • Chromatin, Epigenetics, Genomics & Functional Genomics (332)
  • Development & Differentiation (223)
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  • Plant Biology (75)
  • Post-translational Modifications, Proteolysis & Proteomics (342)
  • Protein Biosynthesis & Quality Control (51)
  • RNA Biology (233)
  • Signal Transduction (336)
  • Stem Cells (93)
  • Structural Biology (193)
  • Synthetic Biology & Biotechnology (21)
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  • Transcription (76)
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