Detecting and Visualising Proteins in Xenopus Embryos
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Examination of the Transcription Factors Acting in Bone Marrow
THESIS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY (PHD) Examination of the transcription factors acting in bone marrow derived macrophages by Gergely Nagy Supervisor: Dr. Endre Barta UNIVERSITY OF DEBRECEN DOCTORAL SCHOOL OF MOLECULAR CELL AND IMMUNE BIOLOGY DEBRECEN, 2016 Table of contents Table of contents ........................................................................................................................ 2 1. Introduction ............................................................................................................................ 5 1.1. Transcriptional regulation ................................................................................................... 5 1.1.1. Transcriptional initiation .................................................................................................. 5 1.1.2. Co-regulators and histone modifications .......................................................................... 8 1.2. Promoter and enhancer sequences guiding transcription factors ...................................... 11 1.2.1. General transcription factors .......................................................................................... 11 1.2.2. The ETS superfamily ..................................................................................................... 17 1.2.3. The AP-1 and CREB proteins ........................................................................................ 20 1.2.4. Other promoter specific transcription factor families ................................................... -
Sexual Dimorphism in Brain Transcriptomes of Amami Spiny Rats (Tokudaia Osimensis): a Rodent Species Where Males Lack the Y Chromosome Madison T
Ortega et al. BMC Genomics (2019) 20:87 https://doi.org/10.1186/s12864-019-5426-6 RESEARCHARTICLE Open Access Sexual dimorphism in brain transcriptomes of Amami spiny rats (Tokudaia osimensis): a rodent species where males lack the Y chromosome Madison T. Ortega1,2, Nathan J. Bivens3, Takamichi Jogahara4, Asato Kuroiwa5, Scott A. Givan1,6,7,8 and Cheryl S. Rosenfeld1,2,8,9* Abstract Background: Brain sexual differentiation is sculpted by precise coordination of steroid hormones during development. Programming of several brain regions in males depends upon aromatase conversion of testosterone to estrogen. However, it is not clear the direct contribution that Y chromosome associated genes, especially sex- determining region Y (Sry), might exert on brain sexual differentiation in therian mammals. Two species of spiny rats: Amami spiny rat (Tokudaia osimensis) and Tokunoshima spiny rat (T. tokunoshimensis) lack a Y chromosome/Sry, and these individuals possess an XO chromosome system in both sexes. Both Tokudaia species are highly endangered. To assess the neural transcriptome profile in male and female Amami spiny rats, RNA was isolated from brain samples of adult male and female spiny rats that had died accidentally and used for RNAseq analyses. Results: RNAseq analyses confirmed that several genes and individual transcripts were differentially expressed between males and females. In males, seminal vesicle secretory protein 5 (Svs5) and cytochrome P450 1B1 (Cyp1b1) genes were significantly elevated compared to females, whereas serine (or cysteine) peptidase inhibitor, clade A, member 3 N (Serpina3n) was upregulated in females. Many individual transcripts elevated in males included those encoding for zinc finger proteins, e.g. -
Single-Nucleotide Human Disease Mutation Inactivates a Blood- Regenerative GATA2 Enhancer
Single-nucleotide human disease mutation inactivates a blood- regenerative GATA2 enhancer Alexandra A. Soukup, … , Sunduz Keles, Emery H. Bresnick J Clin Invest. 2019;129(3):1180-1192. https://doi.org/10.1172/JCI122694. Research Article Hematology Stem cells Graphical abstract Find the latest version: https://jci.me/122694/pdf RESEARCH ARTICLE The Journal of Clinical Investigation Single-nucleotide human disease mutation inactivates a blood-regenerative GATA2 enhancer Alexandra A. Soukup,1,2 Ye Zheng,1,3 Charu Mehta,1,2 Jun Wu,4 Peng Liu,1,2 Miao Cao,1,2 Inga Hofmann,1,5 Yun Zhou,1,6 Jing Zhang,1,6 Kirby D. Johnson,1,2 Kyunghee Choi,4 Sunduz Keles,1,3,7 and Emery H. Bresnick1,2 1UW-Madison Blood Research Program, Department of Cell and Regenerative Biology, Wisconsin Institutes for Medical Research, 2UW Carbone Cancer Center, and 3Department of Statistics, University of Wisconsin–Madison, Madison, Wisconsin, USA. 4Washington University School of Medicine, Saint Louis, Missouri, USA. 5Department of Pediatrics, and 6McArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA. 7Department of Biostatistics and Medical Informatics, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA. The development and function of stem and progenitor cells that produce blood cells are vital in physiology. GATA-binding protein 2 (GATA2) mutations cause GATA-2 deficiency syndrome involving immunodeficiency, myelodysplastic syndrome, and acute myeloid leukemia. GATA-2 physiological activities necessitate that it be strictly regulated, and cell type–specific enhancers fulfill this role. The +9.5 intronic enhancer harbors multiple conserved cis-elements, and germline mutations of these cis-elements are pathogenic in humans. -
The Mouse Gene Expression Database (GXD): 2021 Update
The Jackson Laboratory The Mouseion at the JAXlibrary Faculty Research 2021 Faculty Research 1-8-2021 The mouse Gene Expression Database (GXD): 2021 update. Richard M. Baldarelli Constance M. Smith Jacqueline H. Finger Terry F. Hayamizu Ingeborg J. McCright See next page for additional authors Follow this and additional works at: https://mouseion.jax.org/stfb2021 Part of the Life Sciences Commons, and the Medicine and Health Sciences Commons Authors Richard M. Baldarelli, Constance M. Smith, Jacqueline H. Finger, Terry F. Hayamizu, Ingeborg J. McCright, Jingxia Xu, David R. Shaw, Jonathan S Beal, Olin Blodgett, Jeff Campbell, Lori E. Corbani, Pete J. Frost, Sharon C Giannatto, Dave Miers, James A. Kadin, Joel E Richardson, and Martin Ringwald D924–D931 Nucleic Acids Research, 2021, Vol. 49, Database issue Published online 26 October 2020 doi: 10.1093/nar/gkaa914 The mouse Gene Expression Database (GXD): 2021 update Richard M. Baldarelli, Constance M. Smith, Jacqueline H. Finger, Terry F. Hayamizu, Ingeborg J. McCright, Jingxia Xu, David R. Shaw, Jonathan S. Beal, Olin Blodgett, Jeffrey Campbell, Lori E. Corbani, Pete J. Frost, Sharon C. Giannatto, Dave B. Miers, Downloaded from https://academic.oup.com/nar/article/49/D1/D924/5940496 by Jackson Laboratory user on 27 January 2021 James A. Kadin, Joel E. Richardson and Martin Ringwald * The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA Received September 14, 2020; Revised October 01, 2020; Editorial Decision October 02, 2020; Accepted October 02, 2020 ABSTRACT INTRODUCTION The Gene Expression Database (GXD; www. The longstanding objective of GXD has been to capture informatics.jax.org/expression.shtml) is an exten- and integrate different types of mouse developmental ex- sive and well-curated community resource of mouse pression information, with a focus on endogenous gene ex- developmental gene expression information. -
Xenbase: a Genomic, Epigenomic and Transcriptomic Model Organism Database Kamran Karimi1,*, Joshua D
Published online 20 October 2017 Nucleic Acids Research, 2018, Vol. 46, Database issue D861–D868 doi: 10.1093/nar/gkx936 Xenbase: a genomic, epigenomic and transcriptomic model organism database Kamran Karimi1,*, Joshua D. Fortriede2, Vaneet S. Lotay1, Kevin A. Burns2, Dong Zhou Wang1, Malcom E. Fisher2, Troy J. Pells1, Christina James-Zorn2, Ying Wang1, V.G. Ponferrada2, Stanley Chu1, Praneet Chaturvedi2, Aaron M. Zorn2 and Peter D. Vize1 1Departments of Biological Sciences and Computer Science, University of Calgary, Calgary, Alberta T2N1N4, Canada and 2Cincinnati Children’s Hospital, Division of Developmental Biology, 3333 Burnet Avenue, Cincinnati, OH 45229, USA Received September 13, 2017; Revised September 29, 2017; Editorial Decision October 02, 2017; Accepted October 02, 2017 ABSTRACT unique data generated through the many advantages of this system available to the larger biomedical research commu- Xenbase (www.xenbase.org) is an online resource nity. for researchers utilizing Xenopus laevis and Xeno- In the pre-genome era, Xenbase began with simple pus tropicalis, and for biomedical scientists seeking database modules supporting the Xenopus user commu- access to data generated with these model systems. nity and papers describing research using Xenopus (1). As Content is aggregated from a variety of external re- more powerful resources became available, new expressed sources and also generated by in-house curation of sequence tags and draft genomes were added to build gene- scientific literature and bioinformatic analyses. Over centric features such as ‘Gene Pages’ and these data were the past two years many new types of content have linked to the literature via our Xenopus Anatomical Ontol- been added along with new tools and functionalities ogy, or XAO (2). -
Mat Kadi Tora Tutti O Al Ut Hit Hitta Atuh
MAT KADI TORA TUTTI USO AL20180235194A1 UT HIT HITTA ATUH ( 19) United States (12 ) Patent Application Publication ( 10) Pub . No. : US 2018 /0235194 A1 Fahrenkrug et al. (43 ) Pub . Date : Aug . 23, 2018 ( 54 ) MULTIPLEX GENE EDITING Publication Classification (51 ) Int. Ci. ( 71 ) Applicant: Recombinetics , Inc ., Saint Paul, MN A01K 67/ 027 (2006 . 01 ) (US ) C12N 15 / 90 ( 2006 .01 ) (72 ) Inventors : Scott C . Fahrenkrug, Minneapolis , (52 ) U . S . CI. MN (US ) ; Daniel F . Carlson , CPC .. .. A01K 67 / 0276 (2013 . 01 ) ; C12N 15 / 907 Woodbury , MN (US ) ( 2013 .01 ) ; A01K 67 /0275 ( 2013 .01 ) ; A01K 2267/ 02 (2013 .01 ) ; AOIK 2217 / 15 (2013 .01 ) ; AOIK 2227 / 108 ( 2013 .01 ) ; AOIK 2217 /07 (21 ) Appl. No. : 15 /923 , 951 ( 2013 .01 ) ; A01K 2227/ 101 (2013 .01 ) ; AOIK ( 22 ) Filed : Mar. 16 , 2018 2217 /075 ( 2013 .01 ) (57 ) ABSTRACT Related U . S . Application Data Materials and methods for making multiplex gene edits in (62 ) Division of application No . 14 /698 ,561 , filed on Apr. cells and are presented . Further methods include animals 28 , 2015, now abandoned . and methods of making the same . Methods of making ( 60 ) Provisional application No . 61/ 985, 327, filed on Apr. chimeric animals are presented , as well as chimeric animals . 28 , 2014 . Specification includes a Sequence Listing . Patent Application Publication Aug . 23 , 2018 Sheet 1 of 13 US 2018 / 0235194 A1 GENERATION OF HOMOZYGOUS CATTLE EDITED AT ONE ALLELE USING SINGLE EDITS Edit allele , Raise FO to Mate FO enough times Raise F1s to Mate F1 siblings Clone cell , sexual maturity , to produce enough F1 sexualmaturity , to make Implant, Gestate 2 years generation carrying 2 years homozygous KO , 9 months , birth edited allele to mate 9 months of FO with each other Generation Primary Fibroblasts ? ? ? Time, years FIG . -
Cooperation Between ETS Variant 2 and Jumonji Domain‑Containing 2 Histone Demethylases
5518 MOLECULAR MEDICINE REPORTS 17: 5518-5527, 2018 Cooperation between ETS variant 2 and Jumonji domain‑containing 2 histone demethylases XIAOMENG LI1,2, GENE MOON2, SOOK SHIN2,3, BIN ZHANG1 and RALF JANKNECHT2,3 1China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China; 2Department of Cell Biology, University of Oklahoma Health Sciences Center; 3Stephenson Cancer Center, Oklahoma, OK 73104, USA Received June 2, 2017; Accepted January 3, 2018 DOI: 10.3892/mmr.2018.8507 Abstract. The E26 transformation‑specific (ETS) variant 2 Introduction (ETV2) protein, also designated as ETS‑related 71, is a member of the ETS transcription factor family and is essen- The ETS variant 2 (ETV2) protein, also designated as tial for blood and vascular development in the embryo. The ETS‑related 71 (ER71), is a DNA‑binding transcription role of ETV2 in cancer has not yet been investigated. In the factor (1,2); ETV2 belongs to the E26 transformation‑specific present study, the expression of ETV2 mRNA was identified (ETS) family of proteins, which are characterized by a in a variety of tumor types, including prostate carcinoma. In ~85 amino acid‑long ETS DNA‑binding domain and comprises addition, ETV2 gene amplification was identified in several 28 members in humans (3). The knockout of ETV2 in mice has types of cancer, suggesting that ETV2 plays an oncogenic been reported to cause embryonal lethality around day E9.5, role in tumorigenesis. It was demonstrated that ETV2 indicating that ETV2 is essential during early developmental forms complexes with two histone demethylases: Jumonji stages; in particular, ETV2 is required for the development of domain‑containing (JMJD)2A and JMJD2D; JMJD2A blood and vascular structures (4,5). -
TESI Versió Definitiva Impremta Reedició Corregida 20160330
EVIDÈNCIES EN TEIXIT ADIPÓS D'ALTERACIONS GÈNIQUES DELS VASOS LIMFÀTICS EN L'OBESITAT Alfons Horra Pueyo ADVERTIMENT. L'accés als continguts d'aquesta tesi doctoral i la seva utilització ha de respectar els drets de la persona autora. Pot ser utilitzada per a consulta o estudi personal, així com en activitats o materials d'investigació i docència en els termes establerts a l'art. 32 del Text Refós de la Llei de Propietat Intel·lectual (RDL 1/1996). Per altres utilitzacions es requereix l'autorització prèvia i expressa de la persona autora. En qualsevol cas, en la utilització dels seus continguts caldrà indicar de forma clara el nom i cognoms de la persona autora i el títol de la tesi doctoral. No s'autoritza la seva reproducció o altres formes d'explotació efectuades amb finalitats de lucre ni la seva comunicació pública des d'un lloc aliè al servei TDX. Tampoc s'autoritza la presentació del seu contingut en una finestra o marc aliè a TDX (framing). Aquesta reserva de drets afecta tant als continguts de la tesi com als seus resums i índexs. ADVERTENCIA. El acceso a los contenidos de esta tesis doctoral y su utilización debe respetar los derechos de la persona autora. Puede ser utilizada para consulta o estudio personal, así como en actividades o materiales de investigación y docencia en los términos establecidos en el art. 32 del Texto Refundido de la Ley de Propiedad Intelectual (RDL 1/1996). Para otros usos se requiere la autorización previa y expresa de la persona autora. En cualquier caso, en la utilización de sus contenidos se deberá indicar de forma clara el nombre y apellidos de la persona autora y el título de la tesis doctoral. -
WHITE PAPER in SUPPORT of RESEARCH on GENE REGULATORY NETWORKS (Draft Date: 9/18/2016)
WHITE PAPER IN SUPPORT OF RESEARCH ON GENE REGULATORY NETWORKS (draft date: 9/18/2016) TABLE OF CONTENTS 1. Executive Summary 2. Introduction: Goals of this GRN White Paper 3. The GRN paradigm 4. Impact of GRN science on various research fields 5. What is needed for GRN science 6. Mechanisms to achieve goals 7. Conclusion statement 8. Appendices 1 1. EXECUTIVE SUMMARY Gene regulatory networks (GRNs) constitute the genomic control systems for a broad range of biological processes, including the definition of spatial organization during development, morphogenesis, the differentiation of cell types, and the physiological response to internal and external changes in animals, plants, and prokaryotes. In recent years, the successful solution of several GRNs demonstrated the feasibility of addressing experimentally and computationally the causal control system of a variety of biological processes, opening the gate to a new area of biological sciences. However, despite these important advancements, only a few biological processes have so far been addressed at the GRN level. With this White Paper, we aim to bridge this current gap by illuminating the exciting possibilities of this novel research field, and by providing information and guidelines to facilitate the experimental and computational application of the GRN framework to a variety of biological contexts. The focus of GRN studies is to understand biological function as a consequence of genomic programs. GRN science addresses the mechanism and causality of development and other biological processes in terms of genomic information processing. Even in the simplest of animals, a layer of intricate regulatory commands is needed for development of the body plan and to control spatial and temporal gene expression. -
Mouse Genome Informatics (MGI) Resource: Genetic, Genomic, and Biological Knowledgebase for the Laboratory Mouse Janan T
ILAR Journal, 2017, Vol. 58, No. 1, 17–41 doi: 10.1093/ilar/ilx013 Article Mouse Genome Informatics (MGI) Resource: Genetic, Genomic, and Biological Knowledgebase for the Laboratory Mouse Janan T. Eppig Janan T. Eppig, PhD, is Professor Emeritus at The Jackson Laboratory in Bar Harbor, Maine. Address correspondence to Dr. Janan T. Eppig, The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609 or email [email protected] Abstract The Mouse Genome Informatics (MGI) Resource supports basic, translational, and computational research by providing high-quality, integrated data on the genetics, genomics, and biology of the laboratory mouse. MGI serves a strategic role for the scientific community in facilitating biomedical, experimental, and computational studies investigating the genetics and processes of diseases and enabling the development and testing of new disease models and therapeutic interventions. This review describes the nexus of the body of growing genetic and biological data and the advances in computer technology in the late 1980s, including the World Wide Web, that together launched the beginnings of MGI. MGI develops and maintains a gold-standard resource that reflects the current state of knowledge, provides semantic and contextual data integration that fosters hypothesis testing, continually develops new and improved tools for searching and analysis, and partners with the scientific community to assure research data needs are met. Here we describe one slice of MGI relating to the development of community-wide large-scale mutagenesis and phenotyping projects and introduce ways to access and use these MGI data. References and links to additional MGI aspects are provided. Key words: database; genetics; genomics; human disease model; informatics; model organism; mouse; phenotypes Introduction strains and special purpose strains that have been developed The laboratory mouse is an essential model for understanding provide fertile ground for population studies and the potential human biology, health, and disease. -
Exploring Causal Networks Underlying Fat Deposition and Muscularity In
Peñagaricano et al. BMC Systems Biology (2015) 9:58 DOI 10.1186/s12918-015-0207-6 RESEARCH ARTICLE Open Access Exploring causal networks underlying fat deposition and muscularity in pigs through the integration of phenotypic, genotypic and transcriptomic data Francisco Peñagaricano1,5*, Bruno D. Valente1,2, Juan P. Steibel3, Ronald O. Bates3, Catherine W. Ernst3, Hasan Khatib1 and Guilherme JM Rosa1,4* Abstract Background: Joint modeling and analysis of phenotypic, genotypic and transcriptomic data have the potential to uncover the genetic control of gene activity and phenotypic variation, as well as shed light on the manner and extent of connectedness among these variables. Current studies mainly report associations, i.e. undirected connections among variables without causal interpretation. Knowledge regarding causal relationships among genes and phenotypes can be used to predict the behavior of complex systems, as well as to optimize management practices and selection strategies. Here, we performed a multistep procedure for inferring causal networks underlying carcass fat deposition and muscularity in pigs using multi-omics data obtained from an F2 Duroc x Pietrain resource pig population. Results: We initially explored marginal associations between genotypes and phenotypic and expression traits through whole-genome scans, and then, in genomic regions with multiple significant hits, we assessed gene-phenotype network reconstruction using causal structural learning algorithms. One genomic region on SSC6 showed significant associations with three relevant phenotypes, off-midline10th-rib backfat thickness, loin muscle weight, and average intramuscular fat percentage, and also with the expression of seven genes, including ZNF24, SSX2IP,andAKR7A2. The inferred network indicated that the genotype affects the three phenotypes mainly through the expression of several genes. -
VEGFA: Just One of Multiple Mechanisms for Sex- Specific Av Scular Development Within the Testis? Kevin M
University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Faculty Papers and Publications in Animal Science Animal Science Department 11-2015 VEGFA: Just one of multiple mechanisms for Sex- Specific aV scular Development within the testis? Kevin M. Sargent University of Nebraska-Lincoln Renee M. Sargent University of Nebraska-Lincoln, [email protected] Renata Spuri Gomes University of Nebraska-Lincoln Andrea S. Cupp University of Nebraska-Lincoln, [email protected] Follow this and additional works at: http://digitalcommons.unl.edu/animalscifacpub Part of the Genetics and Genomics Commons, and the Meat Science Commons Sargent, Kevin M.; Sargent, Renee M.; Spuri Gomes, Renata; and Cupp, Andrea S., "VEGFA: Just one of multiple mechanisms for Sex- Specific asV cular Development within the testis?" (2015). Faculty Papers and Publications in Animal Science. 947. http://digitalcommons.unl.edu/animalscifacpub/947 This Article is brought to you for free and open access by the Animal Science Department at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in Faculty Papers and Publications in Animal Science by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. HHS Public Access Author manuscript Author Manuscript Author ManuscriptJ Endocrinol Author Manuscript. Author manuscript; Author Manuscript available in PMC 2016 October 01. Published in final edited form as: J Endocrinol. 2015 November ; 227(2): R31–R50. doi:10.1530/JOE-15-0342. VEGFA: Just one of multiple mechanisms for Sex-Specific Vascular Development within the testis? Kevin M. Sargent, Renee M. McFee, Renata Spuri Gomes, and Andrea S. Cupp Department of Animal Science, University of Nebraska-Lincoln, 3940 Fair Street, Lincoln, Nebraska 68583-0908, USA Abstract Testis development from an indifferent gonad is a critical step in embryogenesis.