Development & Differentiation
- Ack kinase regulates CTP synthase filaments during Drosophila oogenesis
- Todd I Strochlic*,14,
- Kevin P Stavrides1,2,
- Sam V Thomas1,
- Emmanuelle Nicolas3,
- Alana M O'Reilly*,1,2 and
- Jeffrey R Peterson*,1
- 1Cancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA, USA
- 2Epigenetics and Progenitor Cells Keystone Program, Fox Chase Cancer Center, Philadelphia, PA, USA
- 3Genomics Core Facility, Fox Chase Cancer Center, Philadelphia, PA, USA
- 4Department of Biochemistry & Molecular Biology, Drexel University College of Medicine, Philadelphia, PA, USA
- ↵*
Corresponding author. Tel: +1 215 762 3664; E‐mail: Todd.Strochlic{at}drexelmed.edu
Corresponding author. Tel: +1 215 214 1653; E‐mail: Alana.OReilly{at}fccc.edu
Corresponding author. Tel: +1 215 728 3568; Fax: +1 215 728 3574; E‐mail: jeffrey.peterson{at}fccc.edu
DAck kinase is shown to localize to CTP synthase (CTPS) filaments in germ cells of the Drosophila ovary. DAck catalytic activity is required for normal CTPS filament morphology and CTP‐dependent processes such as RNA production, plasma membrane integrity and fertility.
Synopsis
DAck kinase is shown to localize to CTP synthase (CTPS) filaments in germ cells of the Drosophila ovary. DAck catalytic activity is required for normal CTPS filament morphology and CTP‐dependent processes such as RNA production, plasma membrane integrity and fertility.
DAck localizes to cytoplasmic assemblies of the nucleotide biosynthetic enzyme CTPS.
Catalytically active CTPS localizes to filaments.
Flies deficient in DAck catalytic activity have morphologically abnormal CTPS filaments, reduced RNA levels, membrane phospholipid defects and reduced fertility.
EMBO Reports (2014) 15: 1184–1191
- Received February 25, 2014.
- Revision received August 11, 2014.
- Accepted August 12, 2014.
- © 2014 The Authors
- HDAC4 promotes Pax7‐dependent satellite cell activation and muscle regeneration
- Moon‐Chang Choi1,
- Soyoung Ryu1,
- Rui Hao1,
- Bin Wang1,
- Meghan Kapur1,
- Chen‐Ming Fan2 and
- Tso‐Pang Yao*,1
- 1Department of Pharmacology and Cancer Biology, Duke University, Durham, NC, USA
- 2Department of Embryology, Carnegie Institution of Washington, Baltimore, MD, USA
- ↵*Corresponding author. Tel: +1 919 613 8654; E‐mail: tsopang.yao{at}duke.edu
HDAC4 is shown to promote damage‐induced satellite cell (SC) proliferation and muscle regeneration in vivo by stimulating Pax7 expression. It also prevents aberrant lipid accumulation and induction of the brown fat transcription factor Prdm16 in regenerating muscle.
Synopsis
HDAC4 is shown to promote damage‐induced satellite cell (SC) proliferation and muscle regeneration in vivo by stimulating Pax7 expression. It also prevents aberrant lipid accumulation and induction of the brown fat transcription factor Prdm16 in regenerating muscle.
Loss of HDAC4 in SCs reduces expression of Pax7 and its target genes, which in turns inhibits SC proliferation.
Knockdown of HDAC4‐regulated Lix1, a Pax7 target, decreases the proliferative rate of SCs.
HDAC4 inactivation in SCs leads to a prominent reduction of microRNA‐133 and concomitant increase in its target, Prdm16, a master regulator of brown adipogenesis.
EMBO Reports (2014) 15: 1175–1183
- Received June 20, 2014.
- Revision received August 12, 2014.
- Accepted August 14, 2014.
- © 2014 The Authors
- Diversity and convergence in the mechanisms establishing L/R asymmetry in metazoa
- Jean‐Baptiste Coutelis1,2,3,
- Nicanor González‐Morales1,2,3,
- Charles Géminard1,2,3 and
- Stéphane Noselli*,1,2,3
- 1Institut de Biologie Valrose University of Nice Sophia Antipolis, Nice, France
- 2CNRS Institut de Biologie Valrose UMR 7277, Nice, France
- 3INSERM Institut de Biologie Valrose U1091, Nice, France
- ↵*Corresponding author. Tel: +33 4 9207 6433; E‐mail: noselli{at}unice.fr
Defects in left/right body asymmetry lead to severe pathologies in human. This review discusses divergent and common mechanisms of how and when symmetry is broken during embryogenesis in vertebrates and invertebrates, both at the cellular and organism level.
EMBO Reports (2014) 15: 926–937
- Received April 28, 2014.
- Revision received July 3, 2014.
- Accepted July 16, 2014.
- © 2014 The Authors
- SUMO2 is essential while SUMO3 is dispensable for mouse embryonic development
- 1Multidisciplinary Neuroprotection Laboratories, Department of Anesthesiology, Duke University Medical Center, Durham, NC, USA
- 2Department of Cell Biology, Duke University Medical Center, Durham, NC, USA
- 3Department of Neurobiology, Duke University Medical Center, Durham, NC, USA
- ↵*
Corresponding author. Tel: +1 919 684 5576; Fax: +1 919 684 6692; E‐mail: wulf.paschen{at}duke.edu
Corresponding author. Tel: +1 919 684 6573; Fax: +1 919 684 6692; E‐mail: wei.yang{at}duke.edu
This study shows that SUMO2 loss is embryonic lethal while Sumo3−/− mutants lack an overt phenotype, although both isoforms are highly homologous. The data suggest that expression levels and not functional differences between SUMO2 and SUMO3 are critical for embryonic development.
Synopsis
This study shows that SUMO2 loss is embryonic lethal while Sumo3−/− mutants lack an overt phenotype, although both isoforms are highly homologous. The data suggest that expression levels and not functional differences between SUMO2 and SUMO3 are critical for embryonic development.
Sumo3−/− mice are viable
Sumo2−/− embryos die at approximately embryonic day 10.5
SUMO2 is the predominantly expressed SUMO isoform
EMBO Reports (2014) 15: 878–885
- Received January 22, 2014.
- Revision received April 3, 2014.
- Accepted April 22, 2014.
- © 2014 The Authors
- New genes important for development
The genomic revolution and new sequencing technologies are allowing scientists to pick apart the origin of new genes and how they assume vital roles in development, despite their absence from perfectly viable ancestral species.
- © 2014 The Authors
- 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
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