17Th Annual Genes, Brain & Behaviour Meeting Evolutionary
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Deficiency of the Zinc Finger Protein ZFP106 Causes Motor and Sensory
Human Molecular Genetics, 2016, Vol. 25, No. 2 291–307 doi: 10.1093/hmg/ddv471 Advance Access Publication Date: 24 November 2015 Original Article ORIGINAL ARTICLE Deficiency of the zinc finger protein ZFP106 causes Downloaded from https://academic.oup.com/hmg/article/25/2/291/2384594 by guest on 23 September 2021 motor and sensory neurodegeneration Peter I. Joyce1, Pietro Fratta2,†, Allison S. Landman1,†, Philip Mcgoldrick2,†, Henning Wackerhage3, Michael Groves2, Bharani Shiva Busam3, Jorge Galino4, Silvia Corrochano1, Olga A. Beskina2, Christopher Esapa1, Edward Ryder4, Sarah Carter1, Michelle Stewart1, Gemma Codner1, Helen Hilton1, Lydia Teboul1, Jennifer Tucker1, Arimantas Lionikas3, Jeanne Estabel5, Ramiro Ramirez-Solis5, Jacqueline K. White5, Sebastian Brandner2, Vincent Plagnol6, David L. H. Bennet4,AndreyY.Abramov2,LindaGreensmith2,*, Elizabeth M. C. Fisher2,* and Abraham Acevedo-Arozena1,* 1MRC Mammalian Genetics Unit, Harwell, Oxfordshire OX11 0RD, UK, 2UCL Institute of Neurology and MRC Centre for Neuromuscular Disease, Queen Square, London WC1N 3BG, UK, 3Health Sciences, University of Aberdeen, Aberdeen AB25 2ZD, UK, 4Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK, 5Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire CB10 1SA, UK and 6UCL Genetics Institute, London WC1E 6BT, UK *To whom correspondence should be addressed. Email: [email protected] (A.A.)/e.fi[email protected] (E.M.C.F.)/[email protected] (L.G.) Abstract Zinc finger motifs are distributed amongst many eukaryotic protein families, directing nucleic acid–protein and protein–protein interactions. Zinc finger protein 106 (ZFP106) has previously been associated with roles in immune response, muscle differentiation, testes development and DNA damage, although little is known about its specific function. -
Abstracts of Papers Presented at the Tenth Mammalian Genetics And
Genet. Res., Camb. (2000), 76, pp. 199–214. Printed in the United Kingdom # 2000 Cambridge University Press 199 Abstracts of papers presented at the tenth Mammalian Genetics and Deelopment Workshop (Incorporating the Promega Young Geneticists’ Meeting) held at the Institute of Child Health, Uniersity College London on 17–19Noember 1999 " # Edited by: ANDREW J. COPP AND ELIZABETH M. C. FISHER 1Institute of Child Health, Uniersity College London, 30 Guilford Street, London WC1N 1EH, UK # Neurogenetics Unit, Imperial College School of Medicine, St Mary’s Hospital, Norfolk Place, London W2 1PG, UK Sponsored by: The Genetical Society, Promega (UK) Ltd and B&K Universal Group Ltd Evidence for imprinting in type 2 diabetes: detection of Identification of a locus for primary ciliary dyskinesia parent-of-origin effects at the insulin gene on chromosome 19 " " " STEWART HUXTABLE, PHILIP SAKER, LEMA S. L. SPIDEN , M. MEEKS , A. J. WALNE ,H. # # HADDAD, ANDREW HATTERSLEY, MARK BLAU , H. MUSSAFFI-GEORGY ,H. $ % % WALKER and MARK McCARTHY SIMPSON , M. EL FEHAID , M. CHEEBAB ,M. % % Section of Endocrinology, Imperial College School of AL-DABBAGH , H. D. HAMMUM ,R.M. " " Medicine, St Mary’s Hospital, London, UK GARDINER , E. M. K. CHUNG and H. M. " MITCHISON " Variation at the insulin gene (INS) VNTR is impli- Department of Paediatrics, Royal Free and Uniersity cated in type 1 diabetes, polycystic ovarian syndrome College Medical School, Uniersity College London, # and birthweight. Case-control studies inconsistently UK; Schneider Children’s Medical Center of Israel, $ show class III VNTR association with type 2 diabetes, Petech Tika, Israel; School of Medical Sciences, but may result from population stratification. -
The Drosophila Blood-Brain Barrier: Development and Function of a Glial Endothelium
REVIEW ARTICLE published: 14 November 2014 doi: 10.3389/fnins.2014.00365 The Drosophila blood-brain barrier: development and function of a glial endothelium Stefanie Limmer , Astrid Weiler , Anne Volkenhoff , Felix Babatz and Christian Klämbt* Institut für Neuro- und Verhaltensbiologie, Universität Münster, Münster, Germany Edited by: The efficacy of neuronal function requires a well-balanced extracellular ion homeostasis Norman Ruthven Saunders, and a steady supply with nutrients and metabolites. Therefore, all organisms equipped University of Melbourne, Australia with a complex nervous system developed a so-called blood-brain barrier, protecting it Reviewed by: from an uncontrolled entry of solutes, metabolites or pathogens. In higher vertebrates, Alfredo Ghezzi, The University of Texas at Austin, USA this diffusion barrier is established by polarized endothelial cells that form extensive Brigitte Dauwalder, University of tight junctions, whereas in lower vertebrates and invertebrates the blood-brain barrier is Houston, USA exclusively formed by glial cells. Here, we review the development and function of the glial Marko Brankatschk, Max Planck blood-brain barrier of Drosophila melanogaster. In the Drosophila nervous system, at least Institute of Molecular Cell Biology and Genetics, Germany seven morphologically distinct glial cell classes can be distinguished. Two of these glial *Correspondence: classes form the blood-brain barrier. Perineurial glial cells participate in nutrient uptake and Christian Klämbt, Institut für Neuro- establish a first diffusion barrier. The subperineurial glial (SPG) cells form septate junctions, und Verhaltensbiologie, Universität which block paracellular diffusion and thus seal the nervous system from the hemolymph. Münster, Badestr. 9, We summarize the molecular basis of septate junction formation and address the different 48140 Münster, Germany e-mail: [email protected] transport systems expressed by the blood-brain barrier forming glial cells. -
Reproducibility of Behavioral Phenotypes in Mouse Models - a Short History with Critical and Practical Notes
Reproducibility of behavioral phenotypes in mouse models - a short history with critical and practical notes Vootele Voikar Neuroscience Center and Laboratory Animal Center, Helsinki Institute of Life Science Correspondence: Mustialankatu 1 G Helsinki, Finland [email protected] Progress in pre-clinical research is built on endorsed by more than 1000 journals so far, reproducible findings, yet reproducibility has awareness of researchers and the quality of different dimensions and even meanings. Indeed, publications have not been sufficiently improved the terms reproducibility, repeatability, and (13-15). In order to facilitate and enhance replicability are often used interchangeably, implementation of the ARRIVE guidelines, a although each has a distinct definition. Moreover, revised version with exhaustive explanation and reproducibility can be discussed at the level of elaborative documentation was recently published methods, analysis, results, or conclusions (1, 2). (16, 17). Despite these differences in definitions and Paradigm shift. Mice and rats are the most dimensions, the main aim for an individual widely used model animals in basic biomedicine. research group is the ability to develop new However, there has been a drastic change in the studies and hypotheses based on firm and reliable relative use of these two rodent species over time findings from previous experiments. In practice (Figure 1). Historically, the rat was the model of this wish is often difficult to accomplish. In this choice for behavioral studies but from the review, issues affecting reproducibility in the field beginning of 1990s a sharp shift from rats to mice of mouse behavioral phenotyping are discussed. took place. Obviously, this was due to rapid Crisis in reproducibility. -
Sepnetplacements201314213.Pdf
SEPnet Summer Placement Opportunities 2013 1 Dear SEPnet Student I am delighted to be able to present the opportunities available for SEPnet funded work placements in 2013. There are 35 industry placements and 12 research placements in total. Please read through the list of projects carefully – they offer a great opportunity for you to gain valuable work experience this summer. Details about the scheme are set out in the FAQs section below. Please make a note of the deadline dates, in particular, the application deadline of FRIDAY 29 MARCH. If you have any questions you can contact me on my email address below. I wish you all the best with your applications! Veronica Veronica Benson Keep up-to-date with SEPnet Director of Employer Liaison www.facebook.com/SEPnet South-East Physics Network Twitter @SEPhysics [email protected] www.sepnet.ac.uk FAQs How much will I get paid? Successful candidates will receive a bursary of £1,360 which is for eight weeks work in the summer holidays. How does the scheme work? 1. You need to register your details before you start applying. Go to the following page on our website and click on the link called Student Registration Form at: http://www.sepnet.ac.uk/employer_services/summer_internships/information_students.html NB: You will not be able to take up a placement if you have not registered here first. 2. Read the project descriptions in this booklet carefully. We recommend you apply for more than one placement and you may wish to apply for several but remember to target your applications to the projects that really interest you and check the location of the placement to make sure you can get there! 3. -
56Th Annual Teratology Society Meeting
54th Annual Meeting Birth Defects Research (Part A) 106:309–347 (2016) This event has been accredited by the McGill Center for Continuing Health Professional Education. 29th Annual Meeting for Organization of the Teratology Information Specialists (OTIS) June 25–28, 2016 40th Annual Meeting of the Developmental Neurotoxicology Society (DNTS) June 26–29, 2016 All text and graphics are © 2016 by the Teratology Society unless noted. River Walk photo courtesy of Staurt Dee/SACVB. Birth Defects Research (Part A) Clinical and Molecular Teratology 106:309–347 (2016) 310 TERATOLOGY SOCIETY PROGRAM Birth Defects Research (Part A) 106:309–347 (2016) TERATOLOGY SOCIETY PROGRAM 311 Program & Abstracts New Horizons in Birth Defects Research All text and graphics are © 2016 by the Teratology Society unless noted. River Walk photo courtesy of Staurt Dee/SACVB. Birth Defects Research (Part A) 106:309–347 (2016) 312 TERATOLOGY SOCIETY PROGRAM Program Overview FRIDAY, JUNE 24, 2016 12:00 Noon–1:30 PM 12:00 Noon–1:30 PM WEDNESDAY, JUNE 29, 2016 3:00 PM–6:00 PM Student and Postdoctoral Fellow Past Presidents’ and Honorees’ 6:30 AM–7:30 AM Council 1A Meeting Lunch Workshop Luncheon (By Invitation Only) Teratology Society 35th Annual Advancing Your Career in Birth Defects 3:00 PM–6:00 PM 1:30 PM–5:30 PM Volleyball Game Research and Prevention March of Dimes Symposium Registration Open (Advance Registration Required) 7:00 AM–2:30 PM New Approaches to the Treatment of Registration Open 3:00 PM–6:00 PM 1:30 PM–2:00 PM Birth Defects Speaker Ready Room Open 7:00 AM–2:30 PM F. -
Understanding Neurodevelopmental Disorders: the Promise of Regulatory Variation in the 30Utrome
Biological Psychiatry Review Understanding Neurodevelopmental Disorders: The Promise of Regulatory Variation in the 30UTRome Kai A. Wanke, Paolo Devanna, and Sonja C. Vernes ABSTRACT Neurodevelopmental disorders have a strong genetic component, but despite widespread efforts, the specific genetic factors underlying these disorders remain undefined for a large proportion of affected individuals. Given the accessibility of exome sequencing, this problem has thus far been addressed from a protein-centric standpoint; however, protein-coding regions only make up w1% to 2% of the human genome. With the advent of whole genome sequencing we are in the midst of a paradigm shift as it is now possible to interrogate the entire sequence of the human genome (coding and noncoding) to fill in the missing heritability of complex disorders. These new technologies bring new challenges, as the number of noncoding variants identified per individual can be overwhelming, making it prudent to focus on noncoding regions of known function, for which the effects of variation can be predicted and directly tested to assess pathogenicity. The 30UTRome is a region of the noncoding genome that perfectly fulfills these criteria and is of high interest when searching for pathogenic variation related to complex neurodevelopmental disorders. Herein, we review the regulatory roles of the 30UTRome as binding sites for microRNAs or RNA binding proteins, or during alternative polyadenylation. We detail existing evidence that these regions contribute to neuro- developmental disorders and outline strategies for identification and validation of novel putatively pathogenic vari- ation in these regions. This evidence suggests that studying the 30UTRome will lead to the identification of new risk factors, new candidate disease genes, and a better understanding of the molecular mechanisms contributing to neurodevelopmental disorders. -
The Developmental Neurobiology of Autism Spectrum Disorder
The Journal of Neuroscience, June 28, 2006 • 26(26):6897–6906 • 6897 Mini-Review Editor’s Note: Two reviews in this week’s issue examine the rapidly expanding interest in autism research in the neuroscience community. Moldin et al. provide a brief prospective on the overall state of research in autism. DiCicco-Bloom and colleagues summarize their presentations at the Neurobiology of Disease workshop at the 2005 Annual Meeting of the Society for Neuroscience. The Developmental Neurobiology of Autism Spectrum Disorder Emanuel DiCicco-Bloom,1 Catherine Lord,2 Lonnie Zwaigenbaum,3 Eric Courchesne,4,5 Stephen R. Dager,6 Christoph Schmitz,7 Robert T. Schultz,8 Jacqueline Crawley,9 and Larry J. Young10 1Departments of Neuroscience and Cell Biology and Pediatrics (Neurology), Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway, New Jersey 08854, 2University of Michigan Autism and Communication Disorders Center, Departments of Psychology and Psychiatry, University of Michigan, Ann Arbor, MI 48109-2054, 3Department of Pediatrics, McMaster University, Hamilton, Ontario, L8N 3Z5, Canada, 4Department of Neurosciences, University of California, San Diego, La Jolla, California 92093, 5Center for Autism Research, Children’s Hospital Research Center, San Diego, California 92123, 6Departments of Radiology, Psychiatry, and Bioengineering, University of Washington School of Medicine, Seattle, Washington 98105, 7Department of Psychiatry and Neuropsychology, Division of Cellular Neuroscience, Maastricht University, -
A Bridge Between Genes and Brain Activities Juko Ando
【Grant-in-Aid for Scientific Research(S)】 Humanities and Social Sciences (Social sciences) Title of Project：A Twin Study on Sociability and Mental Health: A Bridge between Genes and Brain Activities Juko Ando (Keio University, Faculty of Letters, Professor ) Research Area：behavioral genetics, psychology, brain science, genomics Keyword：twin, genetics, environment, 【Purpose and Background of the Research】 at home and in campus (3) brain structure/function studies by NIRS and At the coming of the dawn of a behavioral MRI neurogenomics era, it has been becoming (4) molecular genetic studies by whole genome rapidly possible to clarify the mechanism in wide SNP scan which how genes and behavior are connected. 【Expected Research Achievements and This can be realized with the integration work Scientific Significance】 of traditional behavioral genetics, recent Genetic and environmental influences on advances of brain sciences, and molecular adaptive social behavior, mental health, and genetics. learning abilities will be clarified. We focus The purpose of this study is to clarify how specifically on “gene-environment interaction” in which genetic effects are manifested sociability, mental health, and related differently in different environmental psychological traits are being developed situations, and “gene- environment correlation” through interactive processes of genes and in which genes are selected by and/or select environment via neurological structures and specific environmental situations. Brain structure and functioning as well as responsible -
Rgma) Induces Neuropathological and Behavioral Changes That Closely Resemble Parkinson's Disease
This Accepted Manuscript has not been copyedited and formatted. The final version may differ from this version. Research Articles: Neurobiology of Disease Repulsive guidance molecule a (RGMa) induces neuropathological and behavioral changes that closely resemble Parkinson's disease J.a. Korecka1, E. B. Moloney1, R. Eggers1, B. Hobo1, S. Scheffer1, N. Ras-Verloop1, R.j. Pasterkamp2, D.f. Swaab3, A.b. Smit4, R.e. Van Kesteren4, K. Bossers1 and J. Verhaagen1,4 1Department of Regeneration of Sensorimotor Systems, Netherlands Institute for Neuroscience, An Institute of the Royal Netherlands Academy of Arts and Sciences, Meibergdreef 47, 1105 BA, Amsterdam, The Netherlands 2Department of Translational Neuroscience, Brain Center Rudolf Magnus, Utrecht University, Universiteitsweg 100, 3584 CG, Utrecht, The Netherlands 3Department of Neuropsychiatric Disorders, Netherlands Institute for Neuroscience, An Institute of the Royal Netherlands Academy of Arts and Sciences, Meibergdreef 47, 1105 BA, Amsterdam, The Netherlands 4Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, Vrije Universiteit Amsterdam, De Boelelaan 1085-1087, 1081 HV, The Netherlands DOI: 10.1523/JNEUROSCI.0084-17.2017 Received: 8 January 2017 Revised: 12 July 2017 Accepted: 11 August 2017 Published: 21 August 2017 Author contributions: JK- experimental design, experimental execution, acquiring data, analyzing data, writing the manuscript; EM- experimental execution, acquiring data, analyzing data, writing the manuscript; RE- experimental execution, experimental design; BH-experimental execution; SS- experimental execution, acquiring data, analyzing data; NRV- experimental execution, acquiring data, analyzing data; RP- experimental design, providing reagents; DS- experimental design,; AS- experimental design, ; RK- experimental design,; KB- experimental design, experimental execution, help with analyzing the data, writing the manuscript; JV- experimental design, writing the manuscript Conflict of Interest: The authors declare no competing financial interests. -
Depression-Associated Gene Negr1-Fgfr2 Pathway Is Altered by Antidepressant Treatment
cells Article Depression-Associated Gene Negr1-Fgfr2 Pathway Is Altered by Antidepressant Treatment Lucia Carboni 1,* , Francesca Pischedda 2, Giovanni Piccoli 2, Mario Lauria 3,4 , Laura Musazzi 5 , Maurizio Popoli 6, Aleksander A. Mathé 7 and Enrico Domenici 2,4 1 Department of Pharmacy and Biotechnology, Alma Mater Studiorum Università di Bologna, 40126 Bologna, Italy 2 Department of Cellular, Computational and Integrative Biology, University of Trento, 38123 Trento, Italy; [email protected] (F.P.); [email protected] (G.P.); [email protected] (E.D.) 3 Department of Mathematics, University of Trento, 38123 Trento, Italy; [email protected] 4 Fondazione The Microsoft Research—University of Trento Centre for Computational and Systems Biology (COSBI), 38068 Rovereto (Trento), Italy 5 School of Medicine and Surgery, University of Milano-Bicocca, 20900 Monza, Italy; [email protected] 6 Laboratory of Neuropsychopharmacology and Functional Neurogenomics, Dipartimento di Scienze Farmaceutiche, Università degli Studi di Milano, 20133 Milano, Italy; [email protected] 7 Karolinska Institutet, Department of Clinical Neuroscience, SE-11221 Stockholm, Sweden; [email protected] * Correspondence: [email protected]; Tel.: +39-051-209-1793 Received: 30 June 2020; Accepted: 28 July 2020; Published: 31 July 2020 Abstract: The Negr1 gene has been significantly associated with major depression in genetic studies. Negr1 encodes for a cell adhesion molecule cleaved by the protease Adam10, thus activating Fgfr2 and promoting neuronal spine plasticity. We investigated whether antidepressants modulate the expression of genes belonging to Negr1-Fgfr2 pathway in Flinders sensitive line (FSL) rats, in a corticosterone-treated mouse model of depression, and in mouse primary neurons. -
The Social Structure, Ecology and Pathogens of Bats in the UK
The Social Structure, Ecology and Pathogens of Bats in the UK Submitted by Thomas Adam August to the University of Exeter as a thesis for the degree of Doctor of Philosophy in Biological Sciences In September 2012 This thesis is available for library use on the understanding that it is copyright material and that no quotation from the thesis may be published without proper acknowledgement. I certify that all material in this thesis which is not my own work has been identified and that no material has previously been submitted and approved for the award of a degree by this or any other university. Signature: ………………………………………………………….. 1 2 Dedicated to the memory of Charles William Stewart Hartley 3 4 Abstract This thesis examines the ecology, parasites and pathogens of three insectivorous bat species in Wytham Woods, Oxfordshire; Myotis nattereri (Natterer’s bat), M. daubentonii (Daubenton’s bat) and Plecotus auritus (Brown long-eared bat). The population structure was assessed by monitoring associations between ringed individuals, utilising recent advances in social network analysis. Populations of both M. daubentonii and M. nattereri were found to subdivide into tight-knit social groups roosting within small areas of a continuous woodland (average minimum roost home range of 0.23km2 and 0.17km2 respectively). If this population structure is a general attribute of these species it may make them more sensitive to small scale habitat change than previously thought and has implications for how diseases may spread through the population. M. daubentonii had a strong preference for roosts close to water, away from woodland edge and in areas with an easterly aspect.