Development & Differentiation
- Neurogenesis during development of the vertebrate central nervous system
- ↵*
Corresponding author. Tel: +49 351 210 1500; Fax: +49 351 210 1600; E‐mail: Paridaen{at}mpi-cbg.de
Corresponding author. Tel: +49 351 210 1500; Fax: +49 351 210 1600; E‐mail: Huttner{at}mpi-cbg.de
This review discusses recent insights into the mechanisms that regulate vertebrate embryonic neurogenesis, including asymmetric cell division, transcriptional and epigenetic regulation, and signaling pathways.
- Received January 8, 2014.
- Revision received February 17, 2014.
- Accepted February 17, 2014.
- © 2014 The Authors
- ↵*
Corresponding author. Tel: +49 351 210 1500; Fax: +49 351 210 1600; E‐mail: Paridaen{at}mpi-cbg.de
- Myc and differentiation: going against the current
A study in this issue reveals an unexpected neurogenic function of MYC in the intact‐polarized chick neural tube. It shows that Myc represses Notch signaling and promotes asymmetric neurogenic cell divisions.
- © 2014 The Authors
- MYC proteins promote neuronal differentiation by controlling the mode of progenitor cell division
- Nikolay Zinin1,†,
- Igor Adameyko2,†,
- Margareta Wilhelm1,
- Nicolas Fritz2,
- Per Uhlén2,
- Patrik Ernfors2 and
- Marie Arsenian Henriksson*,1
- 1Department of Microbiology, Tumor and Cell Biology (MTC) Karolinska Institutet, Stockholm, Sweden
- 2Department of Medical Biochemistry and Biophysics (MBB), Karolinska Institutet, Stockholm, Sweden
- ↵*Corresponding author: Tel: +46 8 524 86205; Fax: +46 8 330744; E‐mail: marie.henriksson{at}ki.se.
-
↵† 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
- 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.
- Dedifferentiation and reprogramming: origins of cancer stem cells
- ↵*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.
EMBO Reports (2014) 15, 244–253
- Received November 21, 2013.
- Revision received January 14, 2014.
- Accepted January 21, 2014.
- © 2014 The Authors
- Ars Moriendi; the art of dying well – new insights into the molecular pathways of necroptotic cell death
- 1The Walter and Eliza Hall Institute of Medical Research, Parkville, Vic., Australia
- 2Department of Medical Biology, University of Melbourne, Parkville, Vic., Australia
- ↵*
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.
EMBO Reports (2014) 15, 155–164
- Received September 10, 2013.
- Revision received December 6, 2013.
- Accepted December 10, 2013.
- © 2014 The Authors
- The SCFSlimb E3 ligase complex regulates asymmetric division to inhibit neuroblast overgrowth
- Song Li1,2,
- Cheng Wang1,
- Edwin Sandanaraj3,4,
- Sherry S Y Aw18,
- Chwee T Koe1,2,
- Jack J L Wong2,5,
- Fengwei Yu1,2,5,
- Beng T Ang3,4,6,
- Carol Tang4,6,7 and
- Hongyan Wang*,1,2,6
- 1Neuroscience & Behavioral Disorders Program, Duke‐National University of Singapore Graduate Medical School Singapore, Singapore City, Singapore
- 2NUS Graduate School for Integrative Sciences and Engineering National University of Singapore, Singapore City, Singapore
- 3Singapore Institute for Clinical Sciences A*STAR, Singapore City, Singapore
- 4National Neuroscience Institute, Singapore City, Singapore
- 5Temasek Life Sciences Laboratory and Department of Biological Sciences, National University of Singapore, Singapore City, Singapore
- 6Department of Physiology, Yong Loo Lin School of Medicine National University of Singapore, Singapore City, Singapore
- 7Division of Medical Sciences, Humphrey Oei Institute of Cancer Research National Cancer Centre, Singapore City, Singapore
- 8Institute of Molecular and Cell Biology, Singapore City, Singapore
- ↵*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.
EMBO Reports (2014) 15, 165–174
- Received September 9, 2013.
- Revision received November 18, 2013.
- Accepted November 19, 2013.
- © 2014 The Authors
- Msd1/SSX2IP‐dependent microtubule anchorage ensures spindle orientation and primary cilia formation
- 1Laboratory of Cell Regulation UK, London Research Institute, London, UK
- 2Department of Cell and Developmental Biology, University College London, London, UK
- 3William Harvey Research Institute Barts and The London Queen Mary's School of Medicine and Dentistry, London, UK
- ↵*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.
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.
- Cellular dynamics in the muscle satellite cell niche
- 1 Sprott Center for Stem Cell Research, Ottawa Hospital Research Institute, 501 Smyth Road, Ottawa, Ontario, K1H 8L6, Canada
- 2 Faculty of Medicine, Department of Cellular and Molecular Medicine, University of Ottawa, 451 Smyth Road, Ottawa, Ontario, K1H 8M5, Canada
- ↵*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.
- Received September 5, 2013.
- Accepted October 21, 2013.
- Copyright © 2013 European Molecular Biology Organization
- Tightly controlled WRKY23 expression mediates Arabidopsis embryo development
- Wim Grunewald*,1,2,†,
- Ive De Smet*,1,2,3,†,
- Bert De Rybel4,
- Helene S Robert1,2,
- Brigitte van de Cotte1,2,
- Viola Willemsen5,
- Godelieve Gheysen6,
- Dolf Weijers4,
- Jiří Friml1,2 and
- Tom Beeckman1,2
- 1 Department of Plant Systems Biology, VIB, and Bioinformatics, Ghent University, 9052, Ghent, Belgium
- 2 Department of Plant Biotechnology and Bioinformatics, Ghent University, 9052, Ghent, Belgium
- 3 Plant and Crop Sciences Division, School of Biosciences, University of Nottingham, LE12 5RD, Loughborough, UK
- 4 Laboratory of Biochemistry, Wageningen University, 6703 HA, Wageningen, The Netherlands
- 5 Plant Developmental Biology Wageningen University, 6700 AP, Wageningen, The Netherlands
- 6 Department Molecular Biotechnology, Faculty of Bioscience Engineering, Ghent University, 9000, Ghent, Belgium
- ↵*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
-
↵† 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.
- Received March 21, 2013.
- Revision received October 4, 2013.
- Accepted October 4, 2013.
- Copyright © 2013 European Molecular Biology Organization
- Autophagy in Myf5+ progenitors regulates energy and glucose homeostasis through control of brown fat and skeletal muscle development
- Nuria Martinez‐Lopez1,2,†,
- Diana Athonvarangkul1,2,†,
- Srabani Sahu1,2,
- Luisa Coletto3,
- Haihong Zong1,4,
- Claire C Bastie1,4,5,
- Jeffrey E Pessin1,2,4,
- Gary J Schwartz1,4,6 and
- Rajat Singh*,1,2,4,7
- 1 Department of Medicine, Albert Einstein College of Medicine, Bronx, New York, 10461, USA
- 2 Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York, 10461, USA
- 3 Venetian Institute of Molecular Medicine, 35129, Padova, Italy
- 4 Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York, 10461, USA
- 5 Division of Metabolic and Vascular Health, Warwick Medical School, Coventry, CV4 7AL, UK
- 6 Department of Neuroscience, Albert Einstein College of Medicine, New York, 10461, USA
- 7 Institute for Aging Studies, Albert Einstein College of Medicine, New York, 10461, USA
- ↵*Corresponding author. Tel:+1 718 430 4118; Fax:+1 718 430 8557; E-mail: rajat.singh{at}einstein.yu.edu
-
↵† 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.
- 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.
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