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  • Neuropeptide Y regulates the hematopoietic stem cell microenvironment and prevents nerve injury in the bone marrow
    Neuropeptide Y regulates the hematopoietic stem cell microenvironment and prevents nerve injury in the bone marrow
    1. Min Hee Park1,2,3,,
    2. Hee Kyung Jin1,4,,
    3. Woo‐Kie Min5,
    4. Won Woo Lee6,
    5. Jeong Eun Lee7,
    6. Haruhiko Akiyama8,
    7. Herbert Herzog9,
    8. Grigori N Enikolopov10,
    9. Edward H Schuchman11 and
    10. Jae‐sung Bae*,1,2,3
    1. 1Stem Cell Neuroplasticity Research Group, Kyungpook National University, Daegu, Korea
    2. 2Department of Physiology, Cell and Matrix Research Institute, School of Medicine, Kyungpook National University, Daegu, Korea
    3. 3Department of Biomedical Science, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University, Daegu, Korea
    4. 4Department of Laboratory Animal Medicine, College of Veterinary Medicine, Kyungpook National University, Daegu, Korea
    5. 5Department of Orthopaedic Surgery, Kyungpook National University Hospital, Daegu, Korea
    6. 6Department of Microbiology and Immunology, Seoul National University College of Medicine, Seoul, Korea
    7. 7Department of Radiation Oncology, Kyungpook National University Hospital, Daegu, Korea
    8. 8Department of Orthopaedics, Kyoto University, Kyoto, Japan
    9. 9Neuroscience Research Program, Garvan Institute of Medical Research, Sydney, NSW, Australia
    10. 10Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, NY, USA
    11. 11Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA
    1. *Corresponding author. Tel: +82 53 420 4815; Fax: +82 53 424 3349; E‐mail: jsbae{at}knu.ac.kr
    1. These authors contributed equally to this work

    Neuropeptide Y maintains hematopoietic stem cells in the bone marrow by instructing the stromal microenvironment.

    Synopsis

    Neuropeptide Y maintains hematopoietic stem cells in the bone marrow by instructing the stromal microenvironment.

    • NPY deficiency causes impairment of HSC survival and bone marrow regeneration.

    • Bone marrow dysfunction by NPY deficiency is due to the destruction of SNS nerve fibers and/or EC reduction.

    • NPY mediates Y1 receptor activation in macrophages, contributing in turn to HSC survival.

    • Treatment with NPY or Y1 agonists prevents cisplatin‐induced bone marrow nerve injury.

    • bone marrow microenvironment
    • hematopoietic stem cell
    • neuropeptide Y
    • regeneration
    • sympathetic nervous system
    • Received September 26, 2014.
    • Revision received March 30, 2015.
    • Accepted April 1, 2015.
    Min Hee Park, Hee Kyung Jin, Woo‐Kie Min, Won Woo Lee, Jeong Eun Lee, Haruhiko Akiyama, Herbert Herzog, Grigori N Enikolopov, Edward H Schuchman, Jae‐sung Bae
  • Talk among yourselves: RNA sponges mediate cross talk between functionally related messenger RNAs
    Talk among yourselves: RNA sponges mediate cross talk between functionally related messenger RNAs
    1. Muhammad S Azam1 and
    2. Carin K Vanderpool (cvanderp{at}life.illinois.edu) 1
    1. 1Department of Microbiology, University of Illinois, Urbana, IL, USA

    When Francis Crick first proposed the central dogma, he predicted that genetic information flows from DNA to RNA and finally to proteins. By this classical concept, the sole purpose of mRNA is to serve as a template for translation. Recent work has expanded our understanding of the function of mRNA well beyond this singular definition. A paper published in this issue sheds more light on the myriad roles mRNAs can play in genetic regulation. Miyakoshi et al (2015a) report an intriguing scenario in Salmonella where a small RNA molecule derived from a larger polycistronic mRNA promotes cross talk between physically unlinked mRNAs via controlling turnover of a global small RNA repressor.

    See also: M Miyakoshi et al and

    D Lalaouna et al

    Recent work shows that bacterial RNAs can act as sponges for sRNAs, thereby altering the regulatory outcome for downstream target mRNAs.

    Muhammad S Azam, Carin K Vanderpool
  • Focus on induced pluripotency and cellular reprogramming
    Thomas Schwarz‐Romond, Evangelos Kiskinis, Kevin Eggan
  • The transcription factor Cabut coordinates energy metabolism and the circadian clock in response to sugar sensing
    The transcription factor Cabut coordinates energy metabolism and the circadian clock in response to sugar sensing
    1. Osnat Bartok1,,
    2. Mari Teesalu2,3,,
    3. Reut Ashwall‐Fluss1,
    4. Varun Pandey1,
    5. Mor Hanan1,
    6. Bohdana M Rovenko2,3,
    7. Minna Poukkula3,
    8. Essi Havula2,3,
    9. Arieh Moussaieff4,5,
    10. Sadanand Vodala6,
    11. Yaakov Nahmias4,5,
    12. Sebastian Kadener*,1 and
    13. Ville Hietakangas*,2,3
    1. 1Biological Chemistry Department, Silberman Institute of Life Sciences The Hebrew University of Jerusalem, Jerusalem, Israel
    2. 2Department of Biosciences, University of Helsinki, Helsinki, Finland
    3. 3Institute of Biotechnology, University of Helsinki, Helsinki, Finland
    4. 4Department of Cell Biology, Silberman Institute of Life Sciences The Hebrew University of Jerusalem, Jerusalem, Israel
    5. 5Center for Bioengineering, The Hebrew University of Jerusalem, Jerusalem, Israel
    6. 6Howard Hughes Medical Institute, Brandeis University, Waltham, MA, USA
    1. * Corresponding author. Tel.: +358 2 94158001; E‐mail: ville.hietakangas{at}helsinki.fi

      Corresponding author. Tel.: +972 2 6585099; E‐mail: skadener{at}mail.huji.ac.il

    1. These authors contributed equally to this work

    Sugar feeding in flies induces specific gene expression but also triggers a repressive branch via transcription factor Cabut. Induction of Cabut alters accumulation of the metabolic enzyme PEPCK and provides a regulatory link between nutrient sensing and the circadian clock.

    Synopsis

    Sugar feeding in flies induces specific gene expression but also triggers a repressive branch via transcription factor Cabut. Induction of Cabut alters accumulation of the metabolic enzyme PEPCK and provides a regulatory link between nutrient sensing and the circadian clock.

    • Transcriptional regulator Cabut is directly activated by Mondo‐Mlx upon sugar feeding.

    • Cabut represses metabolic genes upon sugar feeding.

    • Cabut represses the expression of both isoforms of the phosphoenolpyruvate carboxykinase PEPCK.

    • Deregulation of PEPCK1 contributes to the metabolic imbalance and lethality of mlx mutant animals.

    • Cabut represses the cycling of metabolic target genes of the circadian clock.

    • cabut
    • circadian
    • metabolism
    • nutrient sensing
    • transcription
    • Received February 25, 2015.
    • Revision received March 31, 2015.
    • Accepted April 1, 2015.
    Osnat Bartok, Mari Teesalu, Reut Ashwall‐Fluss, Varun Pandey, Mor Hanan, Bohdana M Rovenko, Minna Poukkula, Essi Havula, Arieh Moussaieff, Sadanand Vodala, Yaakov Nahmias, Sebastian Kadener, Ville Hietakangas
  • SHP2: a new target for pro‐senescence cancer therapies
    SHP2: a new target for pro‐senescence cancer therapies
    1. Manuel Serrano (mserrano{at}cnio.es) 1
    1. 1Spanish National Cancer Research Centre (CNIO), Madrid, Spain

    Cellular senescence is a response to stress that disables cell proliferation and orchestrates an inflammatory process that eliminates damaged cells. The first pro‐senescence drugs for cancer treatment are now a clinical reality, but still few targets have been identified whose inactivation results in cancer cell senescence. Current work published in this issue of The EMBO Journal makes an important contribution to this area by discovering that pharmacological inhibition of the tyrosine phosphatase SHP2 blocks mouse mammary cancer through the induction of senescence (Lan et al, 2015).

    See also: L Lan et al

    Pharmacological inhibition of the tyrosine phosphatase SHP2 blocks mouse mammary cancer through the induction of senescence.

    Manuel Serrano
  • Discrete domains of gene expression in germinal layers distinguish the development of gyrencephaly
    Discrete domains of gene expression in germinal layers distinguish the development of gyrencephaly
    1. Camino de Juan Romero1,
    2. Carl Bruder24,
    3. Ugo Tomasello1,
    4. José Miguel Sanz‐Anquela3 and
    5. Víctor Borrell*,1
    1. 1Instituto de Neurociencias, Consejo Superior de Investigaciones Científicas & Universidad Miguel Hernández, Sant Joan d'Alacant, Spain
    2. 2Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden
    3. 3Service of Pathology, Hospital Universitario “Principe de Asturias”, Alcalá de Henares, Spain
    4. 4GeneData AG, Basel, Switzerland
    1. *Corresponding author. Tel: +34 965 919245; E‐mail: vborrell{at}umh.es

    Complex patterns of gene expression emerge in germinal layers during early cortical development of gyrencephalic animals. These modular expression patterns map the eventual location of folds and fissures.

    Synopsis

    Complex patterns of gene expression emerge in germinal layers during early cortical development of gyrencephalic animals. These modular expression patterns map the eventual location of folds and fissures.

    • Microarray analysis of developing ferret cerebral cortex reveals transcriptomic differences between prospective folds and fissures.

    • Differential gene expression delineates mosaic patterns along proliferative zones prior to the emergence of folds.

    • Some mosaics of gene expression correlate with the prospective location of folds versus fissures.

    • Differentially expressed genes in our microarray analysis include 80% of those mutated in human cortical malformations.

    • folding
    • lissencephaly
    • microarray
    • protocortex
    • transcription factor
    • Received February 4, 2015.
    • Revision received March 26, 2015.
    • Accepted March 27, 2015.

    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.

    Camino de Juan Romero, Carl Bruder, Ugo Tomasello, José Miguel Sanz‐Anquela, Víctor Borrell
  • Sox2, Tlx, Gli3, and Her9 converge on Rx2 to define retinal stem cells in vivo
    <div xmlns="http://www.w3.org/1999/xhtml">Sox2, Tlx, Gli3, and Her9 converge on Rx2 to define retinal stem cells <em>in vivo</em></div>
    1. Robert Reinhardt14,
    2. Lázaro Centanin*,1,,
    3. Tinatini Tavhelidse1,
    4. Daigo Inoue1,
    5. Beate Wittbrodt1,
    6. Jean‐Paul Concordet2,
    7. Juan Ramón Martinez‐Morales3 and
    8. Joachim Wittbrodt*,1
    1. 1Centre for Organismal Studies (COS) Heidelberg, Heidelberg University, Heidelberg, Germany
    2. 2Muséum National d'Histoire Naturelle, Paris, France
    3. 3Centro Andaluz de Biología del Desarrollo (CSIC/UPO/JA), Sevilla, Spain
    4. 4Developmental Genetics, Department of Biomedicine, University of Basel, Basel, Switzerland
    1. * Corresponding author. Tel: +49 6221 546253; E‐mail: lazaro.centanin{at}cos.uni-heidelberg.de

      Corresponding author. Tel: +49 6221 546499; E‐mail: jochen.wittbrodt{at}cos.uni-heidelberg.de

    1. These authors contributed equally to this work

    This study establishes Rx2 as functional determinant of neuro‐epithelial progenitor fate and uncovers the gene regulatory network that governs Rx2 expression.

    Synopsis

    This study establishes Rx2 as functional determinant of neuro‐epithelial progenitor fate and uncovers the gene regulatory network that governs Rx2 expression.

    • Rx2‐positive stem cells can give rise either to neuroretina or to retinal pigmented epithelium.

    • A transcriptional core network of Sox2, TLX, Her9, and Gli3 confines rx2 expression to the peripheral CMZ.

    • Repression of Rx2 (by Gli2 or in Rx2 mutant clones) favors formation of retinal pigmented epithelium.

    • Rx2 balances the fate decision of retinal stem cells towards retinal pigmented epithelium or neural retina.

    • de‐differentiation
    • gene regulation
    • neural stem cells
    • retinal stem cells
    • transcriptional network
    • Received December 1, 2014.
    • Revision received March 21, 2015.
    • Accepted April 1, 2015.

    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.

    Robert Reinhardt, Lázaro Centanin, Tinatini Tavhelidse, Daigo Inoue, Beate Wittbrodt, Jean‐Paul Concordet, Juan Ramón Martinez‐Morales, Joachim Wittbrodt