DOCSLIB.ORG

The Jackson Laboratory Handbook on Genetically Standardized Mice

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Jackson Laboratory Handbook on Genetically Standardized Mice The Jackson Laboratory Handbook on Genetically Standardized Mice The Jackson Laboratory Handbook on Genetically Standardized Mice About The Jackson Laboratory Founded in 1929, The Jackson Laboratory is a non-profit biomedical research institution dedicated to leading the search for tomorrow’s cures. Our mission: We discover precise genomic solutions for disease and empower the global biomedical community in our shared quest to improve human health. The Jackson Laboratory Handbook on Genetically Standardized Mice Sixth Edition Scientific Editor Kevin Flurkey Editor Joanne M. Currer Associate Editors Edward H. Leiter Barbara Witham The Jackson Laboratory Bar Harbor, ME 04609 USA Contributors The Jackson Laboratory Linder, Carol Bar Harbor, ME USA New Mexico Highlands Corrigan, Jennifer University, Corrow, Dorcas Las Vegas, NM USA Currer, Joanne M. Pritchett-Corning, Kathleen Danneman, Peggy Charles River Laboratories Davisson, Muriel Wilmington, MA USA Flurkey, Kevin Harrison, David E. Merriam, Jennifer Strobel, Marge Vonder Haar, Ray Witham, Barbara The Jackson Laboratory Handbook on Genetically Standardized Mice The Jackson Laboratory Bar Harbor, ME 04609 USA © 2009, The Jackson Laboratory. All rights reserved. First Edition: first printing, March 1962 Second Edition: first printing, September 1968; second printing, February 1971 Third Edition: first printing, May 1980 Fourth Edition: first printing, April 1991 Fifth Edition: first printing, August 1997 Sixth Edition: first printing, October 2009 ISBN 978-0-578-04182-7 Registered trademarks of The Jackson Laboratory: JAX® www.jax.org Acknowledgments Many people at The Jackson Laboratory contributed to this edition of The Jackson Laboratory Handbook on Genetically Standardized Mice. We would like to thank the handbook steering committee, whose membership has included Susie Airhart, Carol Bult, Greg Cox, Muriel Davisson, Edward Leiter, Cathy Lutz, John Macauley, Janice Pendola, Brian Soper, Marge Strobel, Laura Trepanier, and Barbara Witham. We also would like to acknowledge the assistance we received from the Technical Information Services staff throughout the duration of this project: Karen Fancher, David Higgins, Peter Kelmenson, Pat North-Hughes, Jennifer Merriam, Jay Palmer, Janice Pendola, James Yeadon, Tanya Lansley, and Yan Yang. And, we want to thank Mike Astle for his pragmatic insight. We especially want to thank Greg Cox, for his extra time and invaluable assistance. And, we want to acknowledge the contribution of Karen Davis, in Multimedia Services, and Michael Greene, in Marketing. Karen created the book cover and provided other invaluable graphical and design help. Michael shaped and managed the production details of the book. We also want to acknowledge the help we received from other reviewers. Specific contributions are noted in individual chapters throughout the book. And we want to recognize employees of The Jackson Laboratory not directly involved in the Handbook. It is because of the contributions of each employee of The Jackson Laboratory that JAX® Mice are so widely used—and so well respected—throughout the global research community; that our animal care, technical support, and other services are so highly regarded; and that our reputation as a research institution remains as exceptional as when the first Handbook was published in 1962. It was a privilege to be involved in this project. Thanks to all. Kevin Flurkey Joanne Currer vii Table of Contents Preface ...................................................................................................................................... xiii Section I: Introduction........................................................................... 1: Why the mouse? ..........................................................................................................1 1.A. From inbred sweet peas to mice ......................................................................................1 1.B. From mice to inbred mice ...............................................................................................2 1.C. From inbred mice to JAX® Mice ....................................................................................3 1.D. JAX® Mice and The Jackson Laboratory ........................................................................3 1.E. It is still about the inbred mouse…..................................................................................7 1.F. For more information… ...................................................................................................7 1.G. References .........................................................................................................................8 2: Some Basic Genetics of the Mouse ..........................................................................9 2.A. Basic information about the laboratory mouse ............................................................10 2.B. The vocabulary of genetic architecture ........................................................................11 2.C. The basic inbred strain experiment—strain differences capture genetic differences .........................................................................................................14 2.D. Linkage analysis..............................................................................................................15 2.E. Genotyping: what it is and how it is used ....................................................................16 2.F. Mapping: definition and tools .......................................................................................17 2.G. Coat color genetics..........................................................................................................20 2.H. For more information… .................................................................................................23 2.I. Resources.........................................................................................................................23 Section II: Using Mice in Research Chapter 3: Categories of Laboratory Mice—Definitions, Uses, Nomenclature ...25 3.A. A few words about nomenclature and terminology .....................................................26 3.A.1. Nomenclature ..................................................................................................26 3.A.2. Strain definition and breeding terminology ..................................................27 3.B. Inbred strains and crosses …..........................................................................................28 3.B.1. Inbred strains, substrains ................................................................................28 3.B.2. Wild-derived inbred strains ............................................................................36 3.B.3. F1 and F2 hybrids ...........................................................................................38 3.B.4. Multi-strain crosses .........................................................................................42 3.C. Strains with single-locus mutations ..............................................................................45 3.C.1. Spontaneous, induced, and genetically engineered mutant strains ..............46 3.C.2. Congenic and conplastic strains .....................................................................54 3.D. Recombinant strain panels .............................................................................................59 3.D.1. Overview .........................................................................................................59 3.D.2. Recombinant inbred (RI) strain panels ..........................................................62 3.D.3. Recombinant congenic (RC) strain panels ....................................................65 3.D.4. Chromosome substitution (CS) strains panels and genome-tagged mice ...67 3.E. Mice with chromosomal aberrations ................................................................................70 3.F. References ..........................................................................................................................73 The Jackson Laboratory Handbook on Genetically Standardized Mice viii Table of Contents Chapter 4: Characteristics of Popular Strains of JAX® Mice, Including Reproductive Performance .......................................................................................... 77 4.A. Strain characteristics (in order of strain name) ............................................................78 4.B. Reproductive performance …......................................................................................138 4.C. References ....................................................................................................................140 Chapter 5: Choosing a Mouse Strain for Research—Considerations and Resources ..................................................................................................................... 149 5.A. General sources of information about mouse strains .................................................150 5.A.1. Resources at The Jackson Laboratory website: www.jax.org ...................150 5.A.2. An example of a strain characteristic comparison from the Mouse Phenome Database (MPD): www.jax.org/phenome ......................151 5.A.3. Other websites ...............................................................................................152 5.A.4. Books .............................................................................................................152
Load more

Recommended publications
  • IDF Patient & Family Handbook
    Immune Deficiency Foundation Patient & Family Handbook for Primary Immunodeficiency Diseases This book contains general medical information which cannot be applied safely to any individual case. Medical knowledge and practice can change rapidly. Therefore, this book should not be used as a substitute for professional medical advice. FIFTH EDITION COPYRIGHT 1987, 1993, 2001, 2007, 2013 IMMUNE DEFICIENCY FOUNDATION Copyright 2013 by Immune Deficiency Foundation, USA. REPRINT 2015 Readers may redistribute this article to other individuals for non-commercial use, provided that the text, html codes, and this notice remain intact and unaltered in any way. The Immune Deficiency Foundation Patient & Family Handbook may not be resold, reprinted or redistributed for compensation of any kind without prior written permission from the Immune Deficiency Foundation. If you have any questions about permission, please contact: Immune Deficiency Foundation, 110 West Road, Suite 300, Towson, MD 21204, USA; or by telephone at 800-296-4433. Immune Deficiency Foundation Patient & Family Handbook for Primary Immunodeficency Diseases 5th Edition This publication has been made possible through a generous grant from Baxalta Incorporated Immune Deficiency Foundation 110 West Road, Suite 300 Towson, MD 21204 800-296-4433 www.primaryimmune.org [email protected] EDITORS R. Michael Blaese, MD, Executive Editor Francisco A. Bonilla, MD, PhD Immune Deficiency Foundation Boston Children’s Hospital Towson, MD Boston, MA E. Richard Stiehm, MD M. Elizabeth Younger, CPNP, PhD University of California Los Angeles Johns Hopkins Los Angeles, CA Baltimore, MD CONTRIBUTORS Mark Ballow, MD Joseph Bellanti, MD R. Michael Blaese, MD William Blouin, MSN, ARNP, CPNP State University of New York Georgetown University Hospital Immune Deficiency Foundation Miami Children’s Hospital Buffalo, NY Washington, DC Towson, MD Miami, FL Francisco A.
    [Show full text]
  • Comparative Life History of the South Temperate Cape Penduline Tit (Anthoscopus Minutus) and North Temperate Remizidae Species
    J Ornithol (2017) 158:569–577 DOI 10.1007/s10336-016-1417-4 ORIGINAL ARTICLE Comparative life history of the south temperate Cape Penduline Tit (Anthoscopus minutus) and north temperate Remizidae species 1,2 1 1 Penn Lloyd • Bernhard D. Frauenknecht • Morne´ A. du Plessis • Thomas E. Martin3 Received: 19 June 2016 / Revised: 22 October 2016 / Accepted: 14 November 2016 / Published online: 22 November 2016 Ó Dt. Ornithologen-Gesellschaft e.V. 2016 Abstract We studied the breeding biology of the south parental nestling care. Consequently, in comparison to the temperate Cape Penduline Tit (Anthoscopus minutus)in other two species, the Cape Penduline Tit exhibits greater order to compare its life history traits with those of related nest attentiveness during incubation, a similar per-nestling north temperate members of the family Remizidae, namely feeding rate and greater post-fledging survival. Its rela- the Eurasian Penduline Tit (Remiz pendulinus) and the tively large clutch size, high parental investment and Verdin (Auriparus flaviceps). We used this comparison to associated high adult mortality in a less seasonal environ- test key predictions of three hypotheses thought to explain ment are consistent with key predictions of the adult latitudinal variation in life histories among bird species— mortality hypothesis but not with key predictions of the the seasonality and food limitation hypothesis, nest pre- seasonality and food limitation hypothesis in explaining dation hypothesis and adult mortality hypothesis. Contrary life history variation among Remizidae species. These to the general pattern of smaller clutch size and lower adult results add to a growing body of evidence of the impor- mortality among south-temperate birds living in less sea- tance of age-specific mortality in shaping life history sonal environments, the Cape Penduline Tit has a clutch evolution.
    [Show full text]
  • Mouse Breeding Colony Management 1. Mouse Reproduction A. General Mouse Information I. the Average Mouse Lives Approximately
    Mouse Breeding Colony Management 1. Mouse Reproduction A. General Mouse Information i. The average mouse lives approximately 2.5 years; however, the reproductive life span of mice is significantly shorter at 7-8 months. ii. Most mice reach sexual maturity (males and females) at 4-7 weeks of age. Younger mice generally produce smaller litters and therefore are not typically mated until they reach 6-8 weeks, of age. Mice that have been housed alone or in same-sex pairs will usually not breed successfully if they are older than 6-8 months. iii. The mouse estrous cycle is 4-5 days in length. Mice cycle continuously throughout the year (non-seasonal breeders). Female mice are only receptive to males when they are in estrus. Mating typically occurs at night (lights off). Ovulation occurs 8-12 hours after the onset of estrous. iv. If fertilization occurs, fetuses can be palpated by day 14. v. Gestation in mice is typically 19-21 days (strain dependent). vi. Parturition in mice may last 1-3 hours and frequently occurs at night. Females will go into estrus within 24 hours of parturition and are sexually receptive during this time. vii. Litter size varies among strains, but averages 4-12 pups. Inbred mice tend to have smaller litters than outbred mice. viii. Mice are typically weaned at 21-28 days or at 10g of body weight. The Purdue Animal Care and Use Committee requires that mouse pups be weaned at 21 days unless PACUC approval is given on an approved animal use protocol. See Policy attached.
    [Show full text]
  • WHIM Syndrome: from Pathogenesis Towards Personalized Medicine and Cure
    Journal of Clinical Immunology (2019) 39:532–556 https://doi.org/10.1007/s10875-019-00665-w CME REVIEW WHIM Syndrome: from Pathogenesis Towards Personalized Medicine and Cure Lauren E. Heusinkveld1,2 & Shamik Majumdar1 & Ji-Liang Gao1 & David H. McDermott1 & Philip M. Murphy1 Received: 22 April 2019 /Accepted: 26 June 2019 /Published online: 16 July 2019 # This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply 2019 Abstract WHIM syndrome is a rare combined primary immunodeficiency disease named by acronym for the diagnostic tetrad of warts, hypogammaglobulinemia, infections, and myelokathexis. Myelokathexis is a unique form of non-cyclic severe congenital neutropenia caused by accumulation of mature and degenerating neutrophils in the bone marrow; monocytopenia and lympho- penia, especially B lymphopenia, also commonly occur. WHIM syndrome is usually caused by autosomal dominant mutations in the G protein-coupled chemokine receptor CXCR4 that impair desensitization, resulting in enhanced and prolonged G protein- and β-arrestin-dependent responses. Accordingly, CXCR4 antagonists have shown promise as mechanism-based treatments in phase 1 clinical trials. This review is based on analysis of all 105 published cases of WHIM syndrome and covers current concepts, recent advances, unresolved enigmas and controversies, and promising future research directions. Keywords Chemokine . CXCL12 . CXCR4 . CXCR2 . myelokathexis . human papillomavirus . plerixafor Historical Background [M:E] ratio with a “shift to the right”); and (3) numerous dysmorphic bone marrow neutrophils having cytoplasmic Myelokathexis was first described as a new type of severe hypervacuolation and hyperlobulated pyknotic nuclear lobes congenital neutropenia in 1964 by Krill and colleagues from connected by long thin strands (Fig.
    [Show full text]
  • A Network of Bhlhzip Transcription Factors in Melanoma: Interactions of MITF, TFEB and TFE3
    A network of bHLHZip transcription factors in melanoma: Interactions of MITF, TFEB and TFE3 Josué A. Ballesteros Álvarez Thesis for the degree of Philosophiae Doctor January 2019 Net bHLHZip umritunarþátta í sortuæxlum: Samstarf milli MITF, TFEB og TFE3 Josué A. Ballesteros Álvarez Ritgerð til doktorsgráðu Leiðbeinandi/leiðbeinendur: Eiríkur Steingrímsson Doktorsnefnd: Margrét H. Ögmundsdóttir Þórarinn Guðjónsson Jórunn E. Eyfjörð Lars Rönnstrand Janúar 2019 Thesis for a doctoral degree at tHe University of Iceland. All rigHts reserved. No Part of tHis Publication may be reProduced in any form witHout tHe Prior permission of the copyright holder. © Josue A. Ballesteros Álvarez. 2019 ISBN 978-9935-9421-4-2 Printing by HáskólaPrent Reykjavik, Iceland 2019 Ágrip StjórnPróteinin MITF , TFEB, TFE3 og TFEC (stundum nefnd MiT-TFE þættirnir) tilheyra bHLHZip fjölskyldu umritunarþátta sem bindast DNA og stjórna tjáningu gena. MITF er mikilvægt fyrir myndun og starfsemi litfruma en ættingjar þess, TFEB og TFE3, stjórna myndun og starfsemi lysósóma og sjálfsáti. Sjálfsát er líffræðilegt ferli sem gegnir mikilvægu hlutverki í starfsemi fruma en getur einnig haft áHrif á myndun og meðHöndlun sjúkdóma. Í verkefni þessu var samstarf MITF, TFE3 og TFEB Próteinanna skoðað í sortuæxlisfrumum og hvaða áhrif þau Hafa á tjáningu hvers annars. Eins og MITF eru TFEB og TFE3 genin tjáð í sortuæxlisfrumum og sortuæxlum; TFEC er ekki tjáð í þessum frumum og var því ekki skoðað í þessu verkefni. Með notkun sérvirkra hindra var sýnt að boðleiðir hafa áhrif á staðsetningu próteinanna þriggja í sortuæxlisfrumum. Umritunarþættir þessir geta bundist skyldum DNA-bindisetum og haft áhrif á tjáningu gena sem eru nauðsynleg fyrir myndun bæði lýsósóma og melanósóma.
    [Show full text]
  • Mouse Models of Human Disease an Evolutionary Perspective Robert L
    170 commentary Evolution, Medicine, and Public Health [2016] pp. 170–176 doi:10.1093/emph/eow014 Mouse models of human disease An evolutionary perspective Robert L. Perlman* Department of Pediatrics, The University of Chicago, 5841 S. Maryland Ave, MC 5058, Chicago, IL 60637, USA *E-mail: [email protected] Received 31 December 2015; revised version accepted 12 April 2016 ABSTRACT The use of mice as model organisms to study human biology is predicated on the genetic and physio- logical similarities between the species. Nonetheless, mice and humans have evolved in and become adapted to different environments and so, despite their phylogenetic relatedness, they have become very different organisms. Mice often respond to experimental interventions in ways that differ strikingly from humans. Mice are invaluable for studying biological processes that have been conserved during the evolution of the rodent and primate lineages and for investigating the developmental mechanisms by which the conserved mammalian genome gives rise to a variety of different species. Mice are less reliable as models of human disease, however, because the networks linking genes to disease are likely to differ between the two species. The use of mice in biomedical research needs to take account of the evolved differences as well as the similarities between mice and humans. KEYWORDS: allometry; cancer; gene networks; life history; model organisms transgenic, knockout, and knockin mice, have If you have cancer and you are a mouse, we can provided added impetus and powerful tools for take good care of you. Judah Folkman [1] mouse research, and have led to a dramatic increase in the use of mice as model organisms.
    [Show full text]
  • Popular Sweeteners and Their Health Effects Based Upon Valid Scientific Data
    Popular Sweeteners and Their Health Effects Interactive Qualifying Project Report Submitted to the Faculty of the WORCESTER POLYTECHNIC INSTITUTE in partial fulfillment of the requirements for the Degree of Bachelor of Science By __________________________________ Ivan Lebedev __________________________________ Jayyoung Park __________________________________ Ross Yaylaian Date: Approved: __________________________________ Professor Satya Shivkumar Abstract Perceived health risks of artificial sweeteners are a controversial topic often supported solely by anecdotal evidence and distorted media hype. The aim of this study was to examine popular sweeteners and their health effects based upon valid scientific data. Information was gathered through a sweetener taste panel, interviews with doctors, and an on-line survey. The survey revealed the public’s lack of appreciation for sweeteners. It was observed that artificial sweeteners can serve as a low-risk alternative to natural sweeteners. I Table of Contents Abstract .............................................................................................................................................. I Table of Contents ............................................................................................................................... II List of Figures ................................................................................................................................... IV List of Tables ...................................................................................................................................
    [Show full text]
  • Laboratory Animal Management: Rodents
    THE NATIONAL ACADEMIES PRESS This PDF is available at http://nap.edu/2119 SHARE Rodents (1996) DETAILS 180 pages | 6 x 9 | PAPERBACK ISBN 978-0-309-04936-8 | DOI 10.17226/2119 CONTRIBUTORS GET THIS BOOK Committee on Rodents, Institute of Laboratory Animal Resources, Commission on Life Sciences, National Research Council FIND RELATED TITLES SUGGESTED CITATION National Research Council 1996. Rodents. Washington, DC: The National Academies Press. https://doi.org/10.17226/2119. Visit the National Academies Press at NAP.edu and login or register to get: – Access to free PDF downloads of thousands of scientific reports – 10% off the price of print titles – Email or social media notifications of new titles related to your interests – Special offers and discounts Distribution, posting, or copying of this PDF is strictly prohibited without written permission of the National Academies Press. (Request Permission) Unless otherwise indicated, all materials in this PDF are copyrighted by the National Academy of Sciences. Copyright © National Academy of Sciences. All rights reserved. Rodents i Laboratory Animal Management Rodents Committee on Rodents Institute of Laboratory Animal Resources Commission on Life Sciences National Research Council NATIONAL ACADEMY PRESS Washington, D.C.1996 Copyright National Academy of Sciences. All rights reserved. Rodents ii National Academy Press 2101 Constitution Avenue, N.W. Washington, D.C. 20418 NOTICE: The project that is the subject of this report was approved by the Governing Board of the National Research Council, whose members are drawn from the councils of the National Academy of Sciences, National Academy of Engineering, and Institute of Medicine. The members of the committee responsible for the report were chosen for their special competences and with regard for appropriate balance.
    [Show full text]
  • Crossbreeding Systems for Small Beef Herds
    ~DMSION OF AGRICULTURE U~l_}J RESEARCH &: EXTENSION Agriculture and Natural Resources University of Arkansas System FSA3055 Crossbreeding Systems for Small Beef Herds Bryan Kutz For most livestock species, Hybrid Vigor Instructor/Youth crossbreeding is an important aspect of production. Intelligent crossbreed- Generating hybrid vigor is one of Extension Specialist - the most important, if not the most ing generates hybrid vigor and breed Animal Science important, reasons for crossbreeding. complementarity, which are very important to production efficiency. Any worthwhile crossbreeding sys- Cattle breeders can obtain hybrid tem should provide adequate levels vigor and complementarity simply by of hybrid vigor. The highest level of crossing appropriate breeds. However, hybrid vigor is obtained from F1s, sustaining acceptable levels of hybrid the first cross of unrelated popula- vigor and breed complementarity in tions. To sustain F1 vigor in a herd, a a manageable way over the long term producer must avoid backcrossing – requires a well-planned crossbreed- not always an easy or a practical thing ing system. Given this, finding a way to do. Most crossbreeding systems do to evaluate different crossbreeding not achieve 100 percent hybrid vigor, systems is important. The following is but they do maintain acceptable levels a list of seven useful criteria for evalu- of hybrid vigor by limiting backcross- ating different crossbreeding systems: ing in a way that is manageable and economical. Table 1 (inside) lists 1. Merit of component breeds expected levels of hybrid vigor or het- erosis for several crossbreeding sys- 2. Hybrid vigor tems. 3. Breed complementarity 4. Consistency of performance Definitions 5. Replacement considerations hybrid vigor – an increase in 6.
    [Show full text]
  • Hypertension, Cardiac Hypertrophy, and Sudden Death in Mice Lacking
    Proc. Natl. Acad. Sci. USA Vol. 94, pp. 14730–14735, December 1997 Medical Sciences Hypertension, cardiac hypertrophy, and sudden death in mice lacking natriuretic peptide receptor A (gene targetingyechocardiographyycardiac dilatationyinterstitial fibrosisyaortic dissection) PAULA M. OLIVER*, JENNIFER E. FOX*, RON KIM*, HOWARD A. ROCKMAN†,HYUNG-SUK KIM*, i ROBERT L. REDDICK‡,KAILASH N. PANDEY§,SHARON L. MILGRAM¶,OLIVER SMITHIES*, AND NOBUYO MAEDA* *Department of Pathology, University of North Carolina, 710 Brinkhous-Bullitt Building, Chapel Hill, NC 27599-7525; Departments of †Medicine and ¶Physiology, University of North Carolina, Chapel Hill, NC 27599; ‡Department of Pathology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284; and §Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, GA 30912 Contributed by Oliver Smithies, October 27, 1997 ABSTRACT Natriuretic peptides, produced in the heart, of blood pressure and in the cardiovascular response to bind to the natriuretic peptide receptor A (NPRA) and cause sustained hypertension we have made mice completely lacking vasodilation and natriuresis important in the regulation of this receptor. Our results demonstrate that NPRA deficiency blood pressure. We here report that mice lacking a functional in mice leads to elevated blood pressures and, particularly in Npr1 gene coding for NPRA have elevated blood pressures and males, to cardiac hypertrophy and sudden death. hearts exhibiting marked hypertrophy with interstitial fibro- sis resembling that seen in human hypertensive heart disease. Echocardiographic evaluation of the mice demonstrated a MATERIALS AND METHODS compensated state of systemic hypertension in which cardiac Gene Targeting. Three electroporations of embryonic stem hypertrophy and dilatation are evident but with no reduction (ES) cells (E14TG2a) were carried out as described (11).
    [Show full text]
  • DOE Human Genome Program Contractor-Grantee Workshop VI November 9-13, 1997 Santa Fe, New Mexico
    CONF-971146 DOE uman ~ ~enome Contact for queries about this publication: Human Genome Program U.S. Department of Energy Office of Biological and Environmental Research ER-72GTN Washington, DC 20585 301/903-6488, Fax: 301/903-8521 E-mail: [email protected] A limited number of print copies are available. Contact: Betty K. Mansfield Oak Ridge National Laboratory 1060 Commerce Park, MS 6480 Oak Ridge, TN 37830 423/576-6669, Fax: 423/574-9888 E-mail: [email protected] An electronic version of this document will be available, after the November 1997 meeting, at the Human Genome Project Information Web site under Publications (http://www.ornl.gov/hgmis). This report has been reproduced directly from the best obtainable copy. Available to DOE and DOE contractors from the Office of Scientific and Technical Information; P.O. Box 62; Oak Ridge, TN 37831. Price information: 423/576-8401. Available to the public from the National Technical Information Service; U.S. Department of Commerce; 5285 Port Royal Road; Springfield, VA 22161. CONF-971146 DOE Human Genome Program Contractor-Grantee Workshop VI November 9-13, 1997 Santa Fe, New Mexico Date Published: October 1997 Prepared for the U.S. Department of Energy Office of Energy Research Office of Biological and Environmental Research Washington, D.C. 20585 under budget and reporting code KP 0404000 Prepared by Hwnan Genome Management Information System Oak Ridge National Laboratory Oak Ridge, 1N 37830-6480 Managed by LOCKHEED MARTIN ENERGY RESEARCH CORP. for the U.S. DEPARTMENT OF ENERGY UNDER CONTRACT DE-AC05-960R22464 Contents Introduction to Contractor-Grantee Workshop VI .............................
    [Show full text]
  • PLANT BREEDING David Luckett and Gerald Halloran ______
    CHAPTER 4 _____________________________________________________________________ PLANT BREEDING David Luckett and Gerald Halloran _____________________________________________________________________ WHAT IS PLANT BREEDING AND WHY DO IT? Plant breeding, or crop genetic improvement, is the production of new, improved crop varieties for use by farmers. The new variety may have higher yield, improved grain quality, increased disease resistance, or be less prone to lodging. Ideally, it will have a new combination of attributes which are significantly better than the varieties already available. The new variety will be a new combination of genes which the plant breeder has put together from those available in the gene pool of that species. It may contain only genes already existing in other varieties of the same crop, or it may contain genes from other distant plant relatives, or genes from unrelated organisms inserted by biotechnological means. The breeder will have employed a range of techniques to produce the new variety. The new gene combination will have been chosen after the breeder first created, and then eliminated, thousands of others of poorer performance. This chapter is concerned with describing some of the more important genetic principles that define how plant breeding occurs and the techniques breeders use. Plant breeding is time-consuming and costly. It typically takes more than ten years for a variety to proceed from the initial breeding stages through to commercial release. An established breeding program with clear aims and reasonable resources will produce a new variety regularly, every couple of years or so. Each variety will be an incremental improvement upon older varieties or may, in rarer circumstances, be a quantum improvement due to some novel gene, the use of some new technique or a response to a new pest or disease.
    [Show full text]