(Lea) Genes in Soybean (Glycine Max (L.) Merr.) Éberson Sanches Calvo Iowa State University

Total Page:16

File Type:pdf, Size:1020Kb

(Lea) Genes in Soybean (Glycine Max (L.) Merr.) Éberson Sanches Calvo Iowa State University Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 1995 Molecular analyses of group 1 late embryogenic abundant (Lea) genes in soybean (Glycine max (L.) Merr.) Éberson Sanches Calvo Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Part of the Genetics Commons, and the Molecular Biology Commons Recommended Citation Calvo, Éberson Sanches, "Molecular analyses of group 1 late embryogenic abundant (Lea) genes in soybean (Glycine max (L.) Merr.) " (1995). Retrospective Theses and Dissertations. 10765. https://lib.dr.iastate.edu/rtd/10765 This Dissertation is brought to you for free and open access by the Iowa State University Capstones, Theses and Dissertations at Iowa State University Digital Repository. It has been accepted for inclusion in Retrospective Theses and Dissertations by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. INFORMATION TO USERS This manuscript has been reproduced from the microfilm master. UMI films the text directfy from the original or copy submitted. Thus, some thesis and dissertation copies are in typewriter face, while others may be £rom any type of conq>uter printer. The quality of this reproduction is dependent upon the qualify of the copy sabmitted. Broken or indistinct print, colored or poor quality illustrations and photographs, print bleedthrough, substandard margins, and inqvoper alignment can adverse^ affect reproduction. In the unlikely event that the author did not send UMI a complete manuscript and there are tnissing pages, these will be noted. Also, if unauthorized copyright material had to be removed, a note wQl indicate the deletion. Oversize materials (e.g., maps, drawings, charts) are reproduced by sectioning the original, beginning at the upper left-hand comer and continuing firom left to right in equal sections with small overlaps. Each original is also photographed in one exposure and is included in reduced form at the back of the book. Photographs included in the original manuscript have been reproduced xerographically in this copy. Higher quality 6" x 9" black and white photogr^hic prints are available for ai^ photogr^hs or illustrations appearing in this copy for an additional charge. Contact UMI directfy to order. A Bell & Howell Information Company 300 North Zeeb Road. Ann Arbor. Mi 48106-1346 USA 313.'761-4700 800/521-0600 Molecular analyses of group 1 late embryogenic abundant (Lea) genes In soybean (Glycine max (L) Merr.) by Eberson Sanches Calvo A Thesis Submitted to the Graduate Faculty in Partial Fulfillment of the Requirements for the Degree of DOCTOR OF PHILOSOPHY Department: Zoology and Genetics Major: Genetics Approved: Signature was redacted for privacy. In Chargje of Major Work Signature was redacted for privacy. For the Major Departm^^t Signature was redacted for privacy. For the Graduate College Iowa State University Ames, Iowa 1995 UMI Number: 9540879 DMI Microform 9540879 Copyright 1995r by DMI Company. All rights reserved. This microform edition is protected against unauthorized copying under Title 17r United States Code. UMI 300 North Zeeb Road Ann Arbor, MI 48103 ii DEDICATION This dissertation marl<s the end of a dream and the start of new ones. I dedicate this worl< to the memory of my friend Emilio Carlos Sachi who could not live long enough to see most of his dreams come true. iii TABLE OF CONTENTS GENERAL INTRODUCTION 1 Rationale 1 Literature Review 2 General Aspects of Plant Embryo Development 2 The LEA Proteins 5 Factors Affecting Gene Expression During Plant Seed Development 6 Abscisic Acid 7 Trans-Acting Elements 11 Cis-Acting Elements 13 Conclusions 19 Dissertation Organization 20 Literature Cited 21 CHAPTER 1: CLONING, MAPPING, AND ANALYSES OF EXPRESSION OF THE Em-LIKE GENE FAMILY IN SOYBEAN (Glycine max (L.) Merr.'> 30 Abstract 30 Introduction 31 Materials and Methods 33 Plant Material 33 ABA and Water Deficit Treatments 33 Isolation of cDNA and Genomic Clones 34 DNA Sequencing and DNA Comparisons 35 RFLP Mapping 36 iv Isolation of DNA and RNA, and Hybridization Analyses 36 Reverse Transcription and PGR 38 Results 38 Screening of cDNA Library 38 Genetic Mapping of the Sle Gene Family 39 Sequence Analyses of Genomic Clones 40 Sle mRNA Accumulation in Embryos 42 Sle mRNA Accumulation in Response to ABA and Water Deficit 44 Discussion 45 Acknowledgments 49 References 49 CHAPTER 2: PROMOTER ANALYSES OF A GROUP 1 LEA GENE FROM SOYBEAN (Glycine max (L) Merr.) IN TRANSGENIC TOBACCO 73 Abstract 73 Introduction 74 Experimental Procedures 76 DNA Sequence and DNA Comparisons 76 Construction of Plasmids 76 PCR Mutagenesis 77 Plant Transformations 79 GUS Assays 79 Results 80 Sle Promoters Contain Several Putative Regulatory Elements 80 The Role of the Distal G-Box Core Motifs 81 V The Role of the Proximal ACGT Core Motif 83 The Role of the SphI Box Motif 84 The Role of the CCACAT Repeats 84 Histochemical Staining of Seeds 86 Discussion 86 References 91 CHAPTERS; GENERAL CONCLUSIONS 112 Literature Cited 115 ACKNOWLEDGMENTS 116 1 GENERAL INTRODUCTION Rationale Five years ago the first solid molecular evidence linking the hormone abscisic acid (ABA) as a major positive regulator of late embryogenesis abundant (Lea; Dure et al., 1993) genes in wheat (Marcotte et al., 1989; Guiltinan et al., 1990) and rice (Mundy et al., 1990) was reported. These results were quite intriguing for those interested in soybean seed development mostly because the pattern of endogenous ABA accumulation in soybean embryos (Ackerson, 1984) appeared to be rather distinct from the pattern observed for rice and wheat embryos (Skriever and Mundy, 1990). Furthermore, evidence already existed showing that ABA could also be a positive regulator of transcription of soybean storage protein genes expressed during the maturation phase of seed development (Bray and Beachy, 1985). Since the molecular cloning and detailed analyses of several soybean storage protein genes were already in progress in other laboratories, we decided to clone a Lea gene from soybean as a means to understand the regulation of late embryogenesis during soybean seed development in a manner comparable to storage protein gene regulation. Probably due to its great economic importance, soybean seed development has been subjected to an array of biochemical and physiological studies (Wilcox, 1987). Thus, the study of gene expression in soybean may ultimately establish several links between phenomena at the molecular level and those at the physiological level. Soybean is still far from being a model genetic organism such as maize or Arabidopsis. However, several plant genes are likely to be redundant even in the small genome of Arabidopsis (the Lea genes are a good exemple), and 2 Will not likely be identified and cloned by standard genetic approaches. Soybean seeds, essentially comprised of embryonic material, offer substantial advantage to the application of several molecular biology approaches that rely on the purification of proteins or other molecules, library constructions, etc. The introduction section of this Dissertation will briefly review our current knowledge of seed development in angiosperms with emphasis on the molecular biological aspects of this process. Literature Review General Aspects of Plant Embryo and Seed Development In angiosperms, embryo and seed development comprise the series of events that take place between double fertilization and the germination process. Double fertilization sets the stage for a series of events characteristic to plant embryo and seed development, which includes the limited pattern formation in the embryo without formation of germ line, the accumulation of storage products in a specialized tissue, and the desiccation and acquisition of a quiescent state by the embryo and seed (Goldberg et al., 1989; Goldberg et al., 1994). Despite the noticeable variation that exists in embryo and seed development between different plant taxa (Esau, 1977), these processes can be generally divided into three phases (Gatehouse and Shirsat, 1993; West and Harada, 1993). The first phase, referred to as early embryogenesis, starts with the double fertilization event. Fertilization of the haploid egg cell nucleus by one of the sperm nuclei initiates embryogenesis, whereas the fertilization of the diploid central cell of the embryo sac originates development of triploid endosperm which nourishes the 3 embryo. Embryo, endosperm and ovule-derived integuments form the seed. It is during this first phase that most of the cell divisions and all of the embryo pattern formation occur (de Jong et al., 1993). Early embryogenesis has been extensively described at the morphological level, but very little is known about the molecular nature of the events occurring during this phase, mostly due to the difficulties associated with the small size of the developing embryo and seed. Nevertheless, the development of somatic embryogenesis and in vitro fertilization systems, and the power of Arabidopsis genetics are already making significant contributions to our understanding of this process (de Jong et al., 1993; Goldberg et al., 1994). The second phase of embryo and seed development is commonly referred to as the maturation phase and, at the molecular level, this phase of development is characterized by intensive synthesis of storage products, mainly starch, proteins, and lipids, that will be used by the germinating embryo and the resulting seedling.
Recommended publications
  • Bioinformatics Approach for Pattern of Myelin-Specific Proteins And
    CORE Metadata, citation and similar papers at core.ac.uk Provided by Qazvin University of Medical Sciences Repository Biotech Health Sci. 2016 November; 3(4):e38278. doi: 10.17795/bhs-38278. Published online 2016 August 16. Research Article Bioinformatics Approach for Pattern of Myelin-Specific Proteins and Related Human Disorders Samiie Pouragahi,1,2,3 Mohammad Hossein Sanati,4 Mehdi Sadeghi,2 and Marjan Nassiri-Asl3,* 1Department of Molecular Medicine, School of Medicine, Qazvin university of Medical Sciences, Qazvin, IR Iran 2Department of Bioinformatics, National Institute of Genetic Engineering and Biotechnology (NIGEB), Tehran, IR Iran 3Department of Pharmacology, Cellular and Molecular Research Center, School of Medicine, Qazvin university of Medical Sciences, Qazvin, IR Iran 4Department of Molecular Genetics, National Institute of Genetic Engineering and Biotechnology (NIGEB), Tehran, IR Iran *Corresponding author: Marjan Nassiri-Asl, School of Medicine, Qazvin University of Medical Sciences, Qazvin, IR Iran. Tel: +98-2833336001, Fax: +98-2833324971, E-mail: [email protected] Received 2016 April 06; Revised 2016 May 30; Accepted 2016 June 22. Abstract Background: Recent neuroinformatic studies, on the structure-function interaction of proteins, causative agents basis of human disease have implied that dysfunction or defect of different protein classes could be associated with several related diseases. Objectives: The aim of this study was the use of bioinformatics approaches for understanding the structure, function and relation- ship of myelin protein 2 (PMP2), a myelin-basic protein in the basis of neuronal disorders. Methods: A collection of databases for exploiting classification information systematically, including, protein structure, protein family and classification of human disease, based on a new approach was used.
    [Show full text]
  • Supplementary Table 1. Down-Regulation of Oligodendrocyte Genes in Schizophrenia
    Supplementary Table 1. Down-regulation of oligodendrocyte genes in schizophrenia Schizophrenia ID Accession Symbol product fold change P value oligodendrocyte transcription factors 36018_at AJ001183 SOX10 SRY (sex determining region Y)-box 10 -1.60 0.001 40624_at U48250 OLIG2 oligodendrocyte lineage transcription factor 2 -1.30 0.019 32187_at AB028973 MYT1 myelin transcription factor 1 1.12 0.571 33539_at W28567 MYEF2 myelin expression factor 2 -1.04 0.887 oligodendrocyte-expressed genes 38558_at M29273 MAG myelin associated glycoprotein -1.76 0.004 41158_at M54927 PLP1 proteolipid protein 1 -1.50 0.011 38499_s_at D28113 MOBP myelin-associated oligodendrocyte basic protein -1.59 0.017 35903_at M63623 OMG oligodendrocyte myelin glycoprotein -1.15 0.022 38653_at D11428 PMP22 peripheral myelin protein 22 -1.28 0.058 38051_at X76220 MAL mal, T-cell differentiation protein -1.11 0.065 612_s_at M19650 CNP 2',3'-cyclic nucleotide 3' phosphodiesterase -1.17 0.072 32538_at S95936 TF transferrin -1.48 0.098 32612_at X04412 GSN gelsolin (amyloidosis, Finnish type) -1.23 0.118 39598_at X04325 GJB1 gap junction protein, beta 1, 32kDa -1.10 0.416 37867_at Z48051 MOG myelin oligodendrocyte glycoprotein 1.39 0.600 35328_at AF055023 NF1 neurofibromin 1 -1.03 0.973 35817_at M13577 MBP myelin basic protein 1.02 1 other oligodendrocyte-related genes 41346_at AJ007583 LARGE like-glycosyltransferase -1.02 0.786 32719_at L41827 NRG1 neuregulin 1 1.07 0.792 1585_at M34309 ERBB3 v-erb-b2 erythroblastic leukemia viral oncogene homolog 3 -1.10 0.294 40387_at U80811
    [Show full text]
  • Basic Protein Detect Circulating Antibodies in Ataxic Horses Siobhan P Ellison Tom J Kennedy Austin Li
    Neuritogenic Peptides Derived from Equine Myelin P2 Basic Protein Detect Circulating Antibodies in Ataxic Horses Siobhan P Ellison Tom J Kennedy Austin Li Corresponding Author: Siobhan P. Ellison, DVM PhD 15471 NW 112th Ave Reddick, Fl 32686 Phone: 352-591-3221 Fax: 352-591-4318 e-mail: [email protected] KEY WORDS: Need Keywords nosis of EPM. No cross-reactivity between the antigens was observed. An evaluation of the agreement between the assays (McNe- ABSTRACT mar’s test) suggests as CRP values increase, the likelihood of a positive MPP ELISA also Polyneuritis equi is an immune-mediated increases. Clinical signs of EPM may be neurodegenerative condition in horses that is due to an immune-mediated polyneuropathy related to circulating demyelinating anti- that involves complex in vivo interactions bodies against equine myelin basic protein with the IL6 pathway because MPP antibod- 2 (MP ). The present study examined the 2 ies and elevated CRP concentrations were presence of circulating demyelinating anti- detected in some horses with S. neurona bodies against neuritogenic peptides of MP 2 sarcocystosis. in sera from horses suspected of equine pro- tozoal encephalomyelitis (EPM), a neurode- INTRODUCTION generative condition in horses that may be Polyneuritis equi is a neurodegenerative immune-mediated. The goals of this study condition in horses that is related to circulat- were to develop serum ELISA tests that may ing demyelinating antibodies against equine identify neuroinflammatory conditions in myelin basic protein 2 (MP2). The clinical horses with EPM and indirectly relate the signs of polyneuritis equi (PE) are simi- pathogenesis of inflammation to IL6 by se- lar to equine protozoal myeloencephalitis rum C-reactive protein (CRP) concentration.
    [Show full text]
  • Supporting Information
    Supporting Information Figure S1. The functionality of the tagged Arp6 and Swr1 was confirmed by monitoring cell growth and sensitivity to hydeoxyurea (HU). Five-fold serial dilutions of each strain were plated on YPD with or without 50 mM HU and incubated at 30°C or 37°C for 3 days. Figure S2. Localization of Arp6 and Swr1 on chromosome 3. The binding of Arp6-FLAG (top), Swr1-FLAG (middle), and Arp6-FLAG in swr1 cells (bottom) are compared. The position of Tel 3L, Tel 3R, CEN3, and the RP gene are shown under the panels. Figure S3. Localization of Arp6 and Swr1 on chromosome 4. The binding of Arp6-FLAG (top), Swr1-FLAG (middle), and Arp6-FLAG in swr1 cells (bottom) in the whole chromosome region are compared. The position of Tel 4L, Tel 4R, CEN4, SWR1, and RP genes are shown under the panels. Figure S4. Localization of Arp6 and Swr1 on the region including the SWR1 gene of chromosome 4. The binding of Arp6- FLAG (top), Swr1-FLAG (middle), and Arp6-FLAG in swr1 cells (bottom) are compared. The position and orientation of the SWR1 gene is shown. Figure S5. Localization of Arp6 and Swr1 on chromosome 5. The binding of Arp6-FLAG (top), Swr1-FLAG (middle), and Arp6-FLAG in swr1 cells (bottom) are compared. The position of Tel 5L, Tel 5R, CEN5, and the RP genes are shown under the panels. Figure S6. Preferential localization of Arp6 and Swr1 in the 5′ end of genes. Vertical bars represent the binding ratio of proteins in each locus.
    [Show full text]
  • Yeast Genome Gazetteer P35-65
    gazetteer Metabolism 35 tRNA modification mitochondrial transport amino-acid metabolism other tRNA-transcription activities vesicular transport (Golgi network, etc.) nitrogen and sulphur metabolism mRNA synthesis peroxisomal transport nucleotide metabolism mRNA processing (splicing) vacuolar transport phosphate metabolism mRNA processing (5’-end, 3’-end processing extracellular transport carbohydrate metabolism and mRNA degradation) cellular import lipid, fatty-acid and sterol metabolism other mRNA-transcription activities other intracellular-transport activities biosynthesis of vitamins, cofactors and RNA transport prosthetic groups other transcription activities Cellular organization and biogenesis 54 ionic homeostasis organization and biogenesis of cell wall and Protein synthesis 48 plasma membrane Energy 40 ribosomal proteins organization and biogenesis of glycolysis translation (initiation,elongation and cytoskeleton gluconeogenesis termination) organization and biogenesis of endoplasmic pentose-phosphate pathway translational control reticulum and Golgi tricarboxylic-acid pathway tRNA synthetases organization and biogenesis of chromosome respiration other protein-synthesis activities structure fermentation mitochondrial organization and biogenesis metabolism of energy reserves (glycogen Protein destination 49 peroxisomal organization and biogenesis and trehalose) protein folding and stabilization endosomal organization and biogenesis other energy-generation activities protein targeting, sorting and translocation vacuolar and lysosomal
    [Show full text]
  • Identification of Potential Key Genes and Pathway Linked with Sporadic Creutzfeldt-Jakob Disease Based on Integrated Bioinformatics Analyses
    medRxiv preprint doi: https://doi.org/10.1101/2020.12.21.20248688; this version posted December 24, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Identification of potential key genes and pathway linked with sporadic Creutzfeldt-Jakob disease based on integrated bioinformatics analyses Basavaraj Vastrad1, Chanabasayya Vastrad*2 , Iranna Kotturshetti 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. 3. Department of Ayurveda, Rajiv Gandhi Education Society`s Ayurvedic Medical College, Ron, Karnataka 562209, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. medRxiv preprint doi: https://doi.org/10.1101/2020.12.21.20248688; this version posted December 24, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Abstract Sporadic Creutzfeldt-Jakob disease (sCJD) is neurodegenerative disease also called prion disease linked with poor prognosis. The aim of the current study was to illuminate the underlying molecular mechanisms of sCJD. The mRNA microarray dataset GSE124571 was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were screened.
    [Show full text]
  • Pathological Relationships Involving Iron and Myelin May Constitute a Shared Mechanism Linking Various Rare and Common Brain Diseases
    Rare Diseases ISSN: (Print) 2167-5511 (Online) Journal homepage: http://www.tandfonline.com/loi/krad20 Pathological relationships involving iron and myelin may constitute a shared mechanism linking various rare and common brain diseases Moones Heidari, Sam H. Gerami, Brianna Bassett, Ross M. Graham, Anita C.G. Chua, Ritambhara Aryal, Michael J. House, Joanna F. Collingwood, Conceição Bettencourt, Henry Houlden, Mina Ryten , John K. Olynyk, Debbie Trinder, Daniel M. Johnstone & Elizabeth A. Milward To cite this article: Moones Heidari, Sam H. Gerami, Brianna Bassett, Ross M. Graham, Anita C.G. Chua, Ritambhara Aryal, Michael J. House, Joanna F. Collingwood, Conceição Bettencourt, Henry Houlden, Mina Ryten , John K. Olynyk, Debbie Trinder, Daniel M. Johnstone & Elizabeth A. Milward (2016) Pathological relationships involving iron and myelin may constitute a shared mechanism linking various rare and common brain diseases, Rare Diseases, 4:1, e1198458, DOI: 10.1080/21675511.2016.1198458 To link to this article: http://dx.doi.org/10.1080/21675511.2016.1198458 © 2016 The Author(s). Published with View supplementary material license by Taylor & Francis Group, LLC© Moones Heidari, Sam H. Gerami, Brianna Bassett, Ross M. Graham, Anita C.G. Chua, Ritambhara Aryal, Michael J. House, Joanna Accepted author version posted online: 22 Submit your article to this journal JunF. Collingwood, 2016. Conceição Bettencourt, PublishedHenry Houlden, online: Mina 22 Jun Ryten, 2016. for the UK Brain Expression Consortium (UKBEC), John K. Olynyk, Debbie Trinder, Daniel M. Johnstone,Article views: and 541 Elizabeth A. Milward. View related articles View Crossmark data Citing articles: 2 View citing articles Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=krad20 Download by: [University of Newcastle, Australia] Date: 17 May 2017, At: 19:57 RARE DISEASES 2016, VOL.
    [Show full text]
  • Whole Cigarette Smoke Condensates Induce Accumulation of Amyloid Beta Precursor Protein with Oxidative Stress in Murine Astrocytes
    toxics Article Whole Cigarette Smoke Condensates Induce Accumulation of Amyloid Beta Precursor Protein with Oxidative Stress in Murine Astrocytes Eun-Jung Park 1,2,3,*, Seung-Woo Jin 3, Hyun-Ji Lim 3, Hyeon-Young Kim 4, Min-Sung Kang 3,5 and Siyoung Yang 6,7 1 East–West Medical Science Research Institute, Kyung Hee Medical Science Research Institute, Kyung Hee University, Seoul 02447, Korea 2 Human Health and Environmental Toxins Research Center, Kyung Hee Medical Science Research Institute, Kyung Hee University, Seoul 02447, Korea 3 Department of Biomedical Science and Technology, Graduate School, Kyung Hee University, Seoul 02447, Korea; [email protected] (S.-W.J.); [email protected] (H.-J.L.); [email protected] (M.-S.K.) 4 Inhalation Toxicology Center for Airborne Risk Factors, Jeonbuk Branch Institute, Korea Institute of Toxicology, Jeongeup 56212, Korea; [email protected] 5 General Toxicology & Research Group, Jeonbuk Branch Institute, Korea Institute of Toxicology, Jeongeup 56212, Korea 6 Department of Pharmacology, Ajou University School of Medicine, Suwon 16499, Korea; [email protected] 7 Degenerative InterDiseases Research Center, Ajou University School of Medicine, Suwon 16499, Korea * Correspondence: [email protected]; Tel.: +82-2-958-1527 Abstract: Although cigarette smoking has been postulated to be a potential risk factor for Alzheimer’s disease (AD), the toxic mechanism is still unclear. Additionally, astrocytes have been identified as a potential target, given they play multiple roles in maintaining normal brain function. In this study, we Citation: Park, E.-J.; Jin, S.-W.; Lim, H.-J.; Kim, H.-Y.; Kang, M.-S.; Yang, S.
    [Show full text]
  • Isolating the Role of Corticosterone in the Hypothalamic-Pituitary-Gonadal Genomic Stress Response
    bioRxiv preprint doi: https://doi.org/10.1101/2020.10.08.330209; this version posted October 9, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-ND 4.0 International license. 1 Isolating the role of corticosterone in the hypothalamic-pituitary-gonadal 2 genomic stress response 3 4 By: Suzanne H. Austin1, *, Rayna Harris1, April M. Booth1, Andrew S. Lang2, Victoria S. Farrar1, 5 Jesse S. Krause1, 3, Tyler A. Hallman4, Matthew MacManes2, and Rebecca M. Calisi1 6 7 1Department of Neurobiology, Physiology, and Behavior, University of California Davis, 1 8 Shields Avenue, Davis, CA, USA, 95616 9 2 Department of Molecular, Cellular and Biomedical Sciences, The University of New 10 Hampshire, 434 Gregg Hall, Durham, NH, USA, 03824 11 3 Department of Biology, University of Nevada, Reno, 1664 N. Virginia Street, Reno, NV, USA, 12 89557-0314 13 4 Department of Fisheries and Wildlife, Oregon State University, 104 Nash Hall, Corvallis, OR 14 97331 15 16 *Current address: 17 Department of Integrative Biology, Oregon State University, 3029 Cordley Hall, Corvallis, OR, 18 USA, 97331; Department of Fisheries and Wildlife, Oregon State University, 104 Nash Hall, 19 Corvallis, OR 97331 20 21 22 23 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.10.08.330209; this version posted October 9, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.
    [Show full text]
  • Supplemental Table 1. List of Candidate Gene Filters Used in the Analysis of Exome Sequencing. MYOPATHY NEUROPATHY MND ABHD5
    BMJ Publishing Group Limited (BMJ) disclaims all liability and responsibility arising from any reliance Supplemental material placed on this supplemental material which has been supplied by the author(s) J Neurol Neurosurg Psychiatry Supplemental table 1. List of candidate gene filters used in the analysis of exome sequencing. MYOPATHY NEUROPATHY MND ABHD5 AAAS AAAS ACADL AARS1 AARS1 ACADM ABCA1 AGT ACADS ABCD1 ALAD ACADVL ABHD12 ALS2 ACTA1 ADCY6 ANG ADSSL1 AFG3L2 APEX1 AGL AIFM1 APOE AGPAT2 AMACR AR AGRN ANG ASAH1 AIRE AP1S1 ATM ALDOA APOA1 ATP7A ALG14 APTX ATXN2 ALG2 ARHGEF10 ATXN3 ALG3 ARL6IP1 B4GALT6 ANKRD2 ARSA BCL11B ANO5 ASAH1 BCL6 ASCC1 ATL1 BICD2 ATGL ATL3 BSCL2 ATP2A1 ATM C19orf12 ATRN ATXN1 C9orf72 B3GALNT2 ATXN10 CCS B3GNT2 ATXN2 CDH13 BAG3 ATXN3 CDH22 BIN1 ATXN7 CHCHD10 BSCL2 B2M CHMP2B BVES B4GALNT1 CNTF CACNA1S BAG3 CNTN4 CAPN3 BCKDHB CNTN6 CASQ1 BSCL2 CRIM1 CAV1 C12orf65 CRYM CAV3 C9orf72 CSNK1G3 CAVIN1 CLP1 CST3 CCDC78 CNTNAP1 CUL4B CDKN1C COX10 CYP2D6 CFL2 COX6A1 DAO Grunseich C, et al. J Neurol Neurosurg Psychiatry 2021;0:1–11. doi: 10.1136/jnnp-2020-325437 BMJ Publishing Group Limited (BMJ) disclaims all liability and responsibility arising from any reliance Supplemental material placed on this supplemental material which has been supplied by the author(s) J Neurol Neurosurg Psychiatry CHAT CPOX DCAF15 CHCHD10 CRYAB DCTN1 CHD7 CTDP1 DIAPH3 CHKB CTSA DISC1 CHN1 CYP27A1 DNAJB2 CHRM3 DARS2 DOC2B CHRNA1 DDHD1 DPP6 CHRNB1 DGUOK DYNC1H1 CHRND DHH EFEMP1 CHRNE DHTKD1 ELP3 CIDEC DMD EPHA4 CLCN1 DNAJB2 EWSR1 CLN3 DNAJC3 EXOSC3 CNBP DNM2 FBLN5 CNTN1 DYNC1H1 FBXO38 COA3 EGR2 FEZF2 COL12A1 EMD FGGY COL13A1 ERCC6 FIG4 COL6A ERCC8 FUS COL6A1 FAH GARS1 COL6A2 FAM126A GBE1 COL6A3 FBLN5 GMPPA COL9A3 FGD4 GRB14 COLQ FGF14 GRN COX10 FIG4 HEXA COX15 FLNC HFE CPT2 FLRT1 HINT1 CRAT FLVCR1 HSPB1 CRPPA FMR1 HSPB3 CRYAB FUS HSPB8 CTNS FXN IGHMBP2 DAG1 GALC ITPR2 DECR1 GAN KDR DES GARS1 KIFAP3 DGUOK GBA2 KLHL9 DIH1 GBE1 LAMA2 DMD GDAP1 LAS1L DMPK GJB1 LIF DNAJB6 GJB3 LIPC DNAJC19 GLA LOX Grunseich C, et al.
    [Show full text]
  • A Seven-Marker Signature and Clinical Outcome in Malignant Melanoma: a Large-Scale Tissue-Microarray Study with Two Independent Patient Cohorts
    A Seven-Marker Signature and Clinical Outcome in Malignant Melanoma: A Large-Scale Tissue-Microarray Study with Two Independent Patient Cohorts Stefanie Meyer1., Thomas J. Fuchs2,6., Anja K. Bosserhoff3, Ferdinand Hofsta¨dter3, Armin Pauer4, Volker Roth5, Joachim M. Buhmann2,6, Ingrid Moll7, Nikos Anagnostou7, Johanna M. Brandner7, Kristian Ikenberg8, Holger Moch8, Michael Landthaler1, Thomas Vogt9", Peter J. Wild8*" 1 Department of Dermatology, University Hospital of Regensburg, Regensburg, Germany, 2 Department of Computer Science, ETH Zurich, Zurich, Switzerland, 3 Institute of Pathology, University Hospital of Regensburg, Regensburg, Germany, 4 Central Tumor Registry Regensburg, Regensburg, Germany, 5 Department of Computer Science, University of Basel, Basel, Switzerland, 6 Competence Center for Systems Physiology and Metabolic Diseases, Institute of Cell Biology, Zurich, Switzerland, 7 Department of Dermatology, University Hospital of Hamburg-Eppendorf, Hamburg, Germany, 8 Institute of Surgical Pathology, University Hospital Zurich, Zurich, Switzerland, 9 Department of Dermatology, Saarland University Hospital, Homburg/Saar, Germany Abstract Background: Current staging methods such as tumor thickness, ulceration and invasion of the sentinel node are known to be prognostic parameters in patients with malignant melanoma (MM). However, predictive molecular marker profiles for risk stratification and therapy optimization are not yet available for routine clinical assessment. Methods and Findings: Using tissue microarrays, we retrospectively analyzed samples from 364 patients with primary MM. We investigated a panel of 70 immunohistochemical (IHC) antibodies for cell cycle, apoptosis, DNA mismatch repair, differentiation, proliferation, cell adhesion, signaling and metabolism. A marker selection procedure based on univariate Cox regression and multiple testing correction was employed to correlate the IHC expression data with the clinical follow-up (overall and recurrence-free survival).
    [Show full text]
  • Program in Human Neutrophils Fails To
    Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 is online at: average * The Journal of Immunology Anaplasma phagocytophilum , 20 of which you can access for free at: 2005; 174:6364-6372; ; from submission to initial decision 4 weeks from acceptance to publication J Immunol doi: 10.4049/jimmunol.174.10.6364 http://www.jimmunol.org/content/174/10/6364 Insights into Pathogen Immune Evasion Mechanisms: Fails to Induce an Apoptosis Differentiation Program in Human Neutrophils Dori L. Borjesson, Scott D. Kobayashi, Adeline R. Whitney, Jovanka M. Voyich, Cynthia M. Argue and Frank R. DeLeo cites 28 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2005/05/03/174.10.6364.DC1 This article http://www.jimmunol.org/content/174/10/6364.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* • Why • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2005 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 25, 2021. The Journal of Immunology Insights into Pathogen Immune Evasion Mechanisms: Anaplasma phagocytophilum Fails to Induce an Apoptosis Differentiation Program in Human Neutrophils1 Dori L.
    [Show full text]