Development & Differentiation
- The RNA‐binding protein Arrest (Bruno) regulates alternative splicing to enable myofibril maturation in Drosophila flight muscle
- Maria L Spletter1,
- Christiane Barz1,
- Assa Yeroslaviz1,
- Cornelia Schönbauer1,
- Irene R S Ferreira1,
- Mihail Sarov2,
- Daniel Gerlach34,
- Alexander Stark3,
- Bianca H Habermann1 and
- Frank Schnorrer*,1
- 1Max Planck Institute of Biochemistry, Martinsried, Germany
- 2Max Planck Institute of Cell Biology and Genetics, Dresden, Germany
- 3Research Institute of Molecular Pathology (IMP) Vienna Biocenter (VBC), Vienna, Austria
- 4Boehringer Ingelheim RCV GmbH & Co KG, Vienna, Austria
- ↵*Corresponding author. Tel: +49 89 8578 2434; E‐mail: schnorrer{at}biochem.mpg.de
Arrest (Bruno) regulates flight muscle‐specific splicing of a large number of genes encoding for sarcomeric proteins. Correct expression of these flight muscle‐specific isoforms is essential to build the contractile apparatus of fibrillar flight muscles.
Synopsis
Arrest (Bruno) regulates flight muscle‐specific splicing of a large number of genes encoding for sarcomeric proteins. Correct expression of these flight muscle‐specific isoforms is essential to build the contractile apparatus of fibrillar flight muscles.
Spalt major induces expression of the RNA binding protein Arrest in flight muscles.
Arrest induces fibrillar muscle‐specific splicing of sarcomeric protein isoforms in flight muscles.
Arrest is essential for normal myofibril maturation and sarcomere growth to prevent hyper‐contraction in adult flight muscles.
EMBO Reports (2015) 16: 178–191
- Received October 27, 2014.
- Revision received November 25, 2014.
- Accepted December 2, 2014.
- © 2014 The Authors. Published under the terms of the CC BY NC ND 4.0 license
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.
- Foxd3 suppresses NFAT‐mediated differentiation to maintain self‐renewal of embryonic stem cells
- 1Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes of Biological Sciences Chinese Academy of Sciences/Shanghai JiaoTong University School of Medicine, Shanghai, China
- 2University of Chinese Academy of Sciences, Beijing, China
- 3Shanghai Stem Cell Institute, Shanghai JiaoTong University School of Medicine, Shanghai, China
- ↵*Corresponding author. Tel: +86 21 5492 3342; E‐mail: yjin{at}sibs.ac.cn
-
↵† These authors contributed equally to this study
This study shows that Foxd3, a pluripotency‐associated transcription factor, interacts with and represses NFAT transcriptional activities by recruiting the co‐repressor Tle4. Thus, Foxd3 represses, while NFATc3 activates, a set of differentiation‐associated genes to maintain the balance between self‐renewal and differentiation in mouse embryonic stem cells.
Synopsis
This study shows that Foxd3, a pluripotency‐associated transcription factor, interacts with and represses NFAT transcriptional activities by recruiting the co‐repressor Tle4. Thus, Foxd3 represses, while NFATc3 activates, a set of differentiation‐associated genes to maintain the balance between self‐renewal and differentiation in mouse embryonic stem cells.
Foxd3 suppresses NFATc3‐induced differentiation in embryonic stem cells by recruiting the co‐repressor Tle4.
Globally, Foxd3 represses, while NFATc3 activates, a set of differentiation‐associated genes in mESCs.
EMBO Reports (2014) 15: 1286–1296
- Received February 17, 2014.
- Revision received September 30, 2014.
- Accepted October 6, 2014.
- © 2014 The Authors
- Epithelial–stromal interaction via Notch signaling is essential for the full maturation of gut‐associated lymphoid tissues
- Yuuki Obata1,2,3,
- Shunsuke Kimura4,
- Gaku Nakato3,
- Keito Iizuka5,
- Yurika Miyagawa5,
- Yutaka Nakamura1,
- Yukihiro Furusawa1,5,
- Machiko Sugiyama6,
- Keiichiro Suzuki7,
- Masashi Ebisawa3,
- Yumiko Fujimura1,5,
- Hisahiro Yoshida6,
- Toshihiko Iwanaga4,
- Koji Hase*,1,5,8 and
- Hiroshi Ohno*,2,3
- 1Division of Mucosal Barriology, International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan
- 2Department of Immune Regulation, Graduate School of Medical and Pharmaceutical Sciences Chiba University, Chiba, Japan
- 3Laboratory for Intestinal Ecosystem, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan
- 4Laboratory of Histology and Cytology, Graduate School of Medicine Hokkaido University, Sapporo, Japan
- 5Department of Biochemistry, Faculty of Pharmacy, Keio University, Tokyo, Japan
- 6Laboratory for Immunogenetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan
- 7AK Project, Graduate School of Medicine Kyoto University, Kyoto, Japan
- 8PRESTO, Japan Science and Technology Agency, Tokyo, Japan
- ↵*
Corresponding author. Tel: +81 5400 2484; E‐mail: hase-kj{at}pha.keio.ac.jp
Corresponding author. Tel: +81 45 503 7031; E‐mail: hiroshi.ohno{at}riken.jp
This study shows that for the full development of gut‐associated lymphoid tissues, stromal cells must induce Notch signaling in the adjacent intestinal epithelium to prevent goblet cell differentiation.
Synopsis
The stromal cells located beneath the follicle‐associated epithelium (FAE) that covers Peyer's patches express Notch ligand. The induction of Notch signaling in FAE is shown to ensure lymphoid follicle compartmentalization in gut‐associated lymphoid tissues by restricting secretory cell differentiation.
This is the first report that demonstrates the contribution of intestinal epithelial cells to the GALT organogenesis.
Notch signaling regulates FAE cellular composition.
Mice lacking epithelial Notch signaling have defects in GALT maturation and antigen‐specific mucosal immune responses.
EMBO Reports (2014) 15: 1297–1304
- Received April 22, 2014.
- Revision received October 2, 2014.
- Accepted October 7, 2014.
- © 2014 The Authors
- Pleiotropic roles of Notch signaling in normal, malignant, and developmental hematopoiesis in the human
- 1McMaster Stem Cell and Cancer Research Institute (SCC‐RI), Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada
- 2Department of Biochemistry and Biomedical Sciences, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada
- ↵*Corresponding author. E‐mail: mbhatia{at}mcmaster.ca
-
↵† These authors contributed equally to this work
The Notch pathway regulates normal and malignant hematopoiesis. This review discusses recent developments in understanding the role of Notch in the human hematopoietic system with special emphasis on hematopoietic initiation from human pluripotent stem cells and regulation within the bone marrow.
EMBO Reports (2014) 15: 1128–1138
- Received March 27, 2014.
- Revision received August 21, 2014.
- Accepted August 27, 2014.
- © 2014 The Authors
- Autophagy‐related gene Atg5 is essential for astrocyte differentiation in the developing mouse cortex
- Shukun Wang1,2,†,
- Baoguo Li1,2,†,
- Huimin Qiao1,2,
- Xiaohui Lv1,
- Qingli Liang1,2,
- Zixiao Shi1,2,
- Wenlong Xia1,
- Fen Ji1 and
- Jianwei Jiao*,1
- 1The State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
- 2University of Chinese Academy of Sciences, Beijing, China
- ↵*Corresponding author. Tel: +86 10 64 806335; E‐mail: jwjiao{at}ioz.ac.cn
-
↵† These authors contributed equally to this work
This study shows that Atg5 promotes astrocyte differentiation during embryonic brain development through autophagic degradation of SOCS2 and activation of the JAK2‐STAT3 pathway.
Synopsis
This study shows that Atg5 promotes astrocyte differentiation during embryonic brain development through autophagic degradation of SOCS2 and activation of the JAK2‐STAT3 pathway.
Atg5 depletion inhibits and Atg5 overexpression enhances astrocyte differentiation.
Atg5 and basal autophagy negatively regulate SOCS2 and activate the JAK2‐STAT3 pathway.
EMBO Reports (2014) 15: 1053–1061
- Received December 10, 2013.
- Revision received July 25, 2014.
- Accepted August 11, 2014.
- © 2014 The Authors
- 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
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