DOCSLIB.ORG

Exploitation of Junior Scientists Must

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Exploitation of Junior Scientists Must correspondence Exploitation of junior scientists must end Sir — There has been a longstanding need Second, exploitation of junior scientists by contrary, the first case was reported in for serious analysis of the genuine ethical their seniors has arguably become campus and city newspapers, and the last problems of exploitation, corruption and commonplace, but is rarely discouraged — was reported at the time to university abuse in science1. Unfortunately, the debate on the contrary, scientists who exploit their officials at the highest level. No action was instead tends to be framed in terms of juniors are richly rewarded. taken against any of the senior faculty ‘fabrication, falsification and plagiarism’. There is considerable anecdotal evidence members involved. In each case he remains On the one hand, we have seen intense for these views. For example, a researcher at in good official standing. and minute public scrutiny of whether a a large private university was reportedly The strictures against open few individuals may have presented false or berated and then struck in the face by her confrontation of offenders are also well misleading scientific information; and on academic supervisor when, after working known. A certain method of ending an the other, independent juries have without pay for two years, she requested a academic career is to protest openly against confirmed that research has been stolen and salary. The senior professor in charge of the mistreatment — however clear the evidence that corruption has occurred at laboratory then fired the researcher in or egregious the offence. universities2,3. Most horrifying of all, Jason response to a court judgement against the Discussing, in this atmosphere, whether Altom, a promising graduate student, felt so supervisor5. or not fabrication, falsification or plagiarism pressured and trapped by academic “abuse” In another example, according to may occur seems to me like asking whether at Harvard that he took his life4. independent sources, senior professors at employees in a company accused of being a So we have an elite society that exploits different universities routinely hire foreign sweatshop pilfer thread or make shoddy junior colleagues to the point of suicide, but postdocs who have to work indefinitely clothes. It is time for scientists of merit to we are choosing to discuss not what is under conditions that they stipulate by address the real issues of concern to the next fundamentally wrong with the system, but refusing to write letters of recommendation. generation of scientists. whether the system produces accurate And in a third example, the chairperson Are incidents such as those I report information at all times. of a university department has been common? Can responsible scientists take Two important points about scientific accused of changing the budgets on grants measures to protect students and junior ethics have not, to my knowledge, been written by junior researchers to support researchers? These are the issues crying out discussed together. First, scientific himself rather than the grant authors. He for attention, not whether data has ever falsification is both rare and severely then allegedly stopped their salaries without been pilfered or if research might be shoddy. punished. This is intrinsic to the nature of notice and demanded that the researchers Troy Shinbrot science: a falsification that has any ghost-write further grant proposals as the Department of Chemical & Biochemical meaningful implications will sooner or price for reinstatement. Engineering, Rutgers University, later be found out as its implications are The atmosphere that would permit a Piscataway, New Jersey 08854, USA examined. Likewise scientists are professor to think that such behaviour 1. Abbott, A. et al. Nature 398, 13–17 (1999). understandably fiercely protective of the could be acceptable seems to be clear 2. Charatan, F. B. Br. Med. J. 315, 501 (1997). 3. Science 265, 463 (1994). perceived value of their product, so evidence that the system is badly broken. 4. Nadis, S. Nature 395, 826 (1998). punishment for falsification is severe. Nor are these incidents obscure. On the 5. Zorn, E. “Chicagoland” p. 1, Chicago Tribune (25 Feb. 1993). The finding of this cross-hybridizing additional key contributors to this Lifting the lid on the band was first published in Garber’s paper2: important discovery. Why is it so hard for “Under stringent hybridization conditions, McGinnis and Lawrence to accept that I, homeobox discovery weak homology with both the 903 and 909 too, may have had a share in it? probes was detected at position 190 kb… Walter Gehring Sir — In reviewing my book, Master These findings are being investigated Biozentrum, University of Basel, Control Genes in Development and further”; and subsequently in McGinnis’s Klingelbergstrasse 70, CH-4056 Basel, Switzerland Evolution, William McGinnis and Peter A. paper3 describing the discovery of the Lawrence1 invoke Lewis Carroll’s remark homeobox: “Garber et al. found a weak McGinnis and Lawrence reply — Gehring that “your view depends on where you’re homology between the 903 cDNA and a site states that there is documentary evidence standing”. The remark is only witty if the to the left of the Antp locus at position 190 that it was he alone of his research group facts are correct. In this review, they are not. on the map in Fig. 1. This site has who appreciated that a weak band on Like many a discovery, that of the subsequently been shown to be part of the Garber’s Southern blot of autumn 1982 was homeobox was sparked by a vague transcription unit of the fushi tarazu gene the first sign of the homeobox. This indication that could either be disregarded as (A. K. and E. H. in preparation)”. evidence consists of the statement in the irrelevant, or followed up. This was a weak Would we have published this finding if November 1983 paper of Garber et al.2 that band on a gel of Richard Garber’s which I had judged it an artefact “lumped into “weak homology was detected between 903 most members of my research group uninterpretable results”? In fact, it was the and 909 probes (Antennapedia cDNAs) and considered to be an artefact, but to me this first sign of the homeobox that caused me position 190 (of the genomic walk that was the first sign of the homeobox. The great excitement. It was McGinnis who included the Antennapedia transcription reviewers claim that “[this band] was analysed this weak homology cleanly and unit)”. However, this paper was submitted attributed to overloading of the gel, lumped determined the sequence of the homeobox. on 18 July 1983, after the significance of the into the ‘uninterpretable results’ category Because of his important contribution, he homeobox cross-hybridization had become and not followed up”. This statement is fully deserved to be first author of the paper clear to everyone in Gehring’s lab — but by incorrect. We reproduced this band and describing the homeobox. Michael Levine, the different route described in our review. documented it in two papers. Atsushi Kuroiwa and Ernst Hafen were In July 1983, the status of homeobox NATURE | VOL 399 | 10 JUNE 1999 | www.nature.com © 1999 Macmillan Magazines Ltd 521 correspondence research was as follows. A few novel giving birth and raising children shortens P, PO Box 9600, 2300 RC Leiden, The Netherlands Drosophila homeobox clones had been life expectancy. But, once you have children, †Biological Gerontology Group, Department of isolated, and one of these was defined as a 3´ the number you have makes no difference Geriatric Medicine and The School of Biological exon of the Ultrabithorax (homeotic) gene. to your life expectancy. Therefore, it is not a Sciences, University of Manchester, 3.239 Stopford All the novel clones mapped to cytogenetic matter of reduced fertility, but a case of ‘to Building, Oxford Road, Manchester M13 9PT, UK regions that were known to contain the two have or have not’. 1. Westendorp, R. G. J. & Kirkwood, T. B. L. Nature 396, 743–746 homeotic gene clusters in flies. The Toon Ligtenberg, Henk Brand (1998). 2. Cummins, J. Nature 397, 557–558 (1999). Department of Oral Biology, Academic Centre for transcripts encoded in these clones were 3. Lund, E., Arnesen, E. & Borgan, J.-K. J. Epidemiol. Community expressed in unique, homeotic-like stripes Dentistry, van der Boechorststraat 7, Health 44, 237–240 (1990). on the anteroposterior axis of developing 1081 BT Amsterdam, The Netherlands 4. Promislow, D. E. L. Nature 396, 719–720 (1998). embryos. So, at the time the 1983 Garber paper was written, it was known in Westendorp and Kirkwood reply — We found1 Gehring’s lab (but only retrospectively) that that aristocratic women had low average Garber’s band was not an artefact. family sizes, the reasons for which are City dwellers must share It is always possible that Gehring sensed discussed by Jim Cummins2. In these or knew in 1982 that Garber’s band was a circumstances, any impairment of fertility is blame on biodiversity crucial clue which should be the basis of likely to result in an increased likelihood of further investigation. However, to our remaining childless. Excluding childless Sir — In your editorial on the debate over knowledge no one heard any such couples from the analysis is therefore genetically modified foods, you say “the suggestion, nothing was done about it, and counterintuitive. In our opinion, the data steady reduction of biodiversity remains a it did not spark the crucial experiments on from the British aristocracy do not support silent witness to the potential of modern the homeobox sequence in Antennapedia Ligtenberg and Brand’s conclusion that “once agriculture to inflict damage on the and other developmental control genes. you have children, the number you have environment and the wildlife it supports” William McGinnis makes no difference to your life expectancy”.
Load more

Recommended publications
  • High-Affinity Binding Sites for the Deformed Protein Are Required for the Function of an Autoregulatory Enhancer of the Deformed Gene
    Downloaded from genesdev.cshlp.org on October 9, 2021 - Published by Cold Spring Harbor Laboratory Press High-affinity binding sites for the Deformed protein are required for the function of an autoregulatory enhancer of the Deformed gene Michael Regulski,*'^ Scott Dessain/ Nadine McGinnis/ and William McGinnis*'^ Departments of Biology' and Molecular Biophysics and Biochemistry^ Yale University, New Haven, Connecticut 06511 USA The homeotic selector gene Deformed [Dfd) is required to specify the identity of head segments during Drosophila development. Previous experiments have shown that for the Dfd segmental identity function to operate in epidermal cells, the Dfd gene must be persistently expressed. One mechanism that provides persistent embryonic expression of Dfd is an autoregulatory circuit. Here, we show that the control of this autoregulatory circuit is likely to be directly mediated by the binding of Dfd protein to an upstream enhancer in Dfd locus DNA. In a 25-kb region around the Dfd transcription unit, restriction fragments with the highest binding affinity for Dfd protein map within the limits of the upstream autoregulatory element at approximately -5 kb. A minimal autoregulatory element, within a 920-bp segment of upstream DNA, has four moderate- to high-affinity binding sites for Dfd protein, with the two highest affinity sites sharing an ATCATTA consensus sequence. Site-specific mutagenesis of these four sites results in an element that has low affinity for Dfd protein when assayed in vitro and is nonfunctional when assayed in embryos. \Key Words: Deformed; autoregulatory circuit; homeo domain, homeotic protein] Received October 26, 1990; revised version accepted December 13, 1990.
    [Show full text]
  • Perspectives
    Copyright 0 1994 by the Genetics Society of America Perspectives Anecdotal, Historical and Critical Commentaries on Genetics Edited by James F. Crow and William F. Dove A Century of Homeosis, A Decade of Homeoboxes William McGinnis Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06520-8114 NE hundred years ago, while the science of genet- ing mammals, and were proposed to encode DNA- 0 ics still existed only in the yellowing reprints of a binding homeodomainsbecause of a faint resemblance recently deceased Moravian abbot, WILLIAMBATESON to mating-type transcriptional regulatory proteins of (1894) coined the term homeosis to define a class of budding yeast and an even fainter resemblance to bac- biological variations in whichone elementof a segmen- terial helix-turn-helix transcriptional regulators. tally repeated array of organismal structures is trans- The initial stream of papers was a prelude to a flood formed toward the identity of another. After the redis- concerning homeobox genes and homeodomain pro- coveryof MENDEL’Sgenetic principles, BATESONand teins, a flood that has channeled into a steady river of others (reviewed in BATESON1909) realized that some homeo-publications, fed by many tributaries. A major examples of homeosis in floral organs and animal skel- reason for the continuing flow of studies is that many etons could be attributed to variation in genes. Soon groups, working on disparate lines of research, have thereafter, as the discipline of Drosophila genetics was found themselves swept up in the currents when they born and was evolving into a formidable intellectual found that their favorite protein contained one of the force enriching many biologicalsubjects, it gradually be- many subtypes of homeodomain.
    [Show full text]
  • A Screen for Modifiers of Dejin-Med Function in Drosophila
    Copyright Q 1995 by the Genetics Society of America A Screen for Modifiers of Dejin-med Function in Drosophila Katherine W. Hardjng,* Gabriel Gellon? Nadine McGinnis* and William M~Ginnis*~~ *Departwnt of Molecular Biophysics and Biochemistry and iDepartment of Biology, Yak University, New Haven Connecticut 06520-8114 Manuscript received February 16, 1995 Accepted for publication May 13, 1995 ABSTRACT Proteins produced by the homeotic genes of the Hox family assign different identities to cells on the anterior/posterior axis. Relatively little is known about the signalling pathways that modulate their activities or the factors with which they interact to assign specific segmental identities. To identify genes that might encode such functions, we performed a screen for second site mutations that reduce the viability of animals carrying hypomorphic mutant alleles of the Drosophila homeotic locus, Deformed. Genes mapping to six complementation groups on the third chromosome were isolatedas modifiers of Defolmd function. Productsof two of these genes, sallimus and moira, have been previously proposed as homeotic activators since they suppress the dominant adult phenotype of Polycomb mutants. Mutations in hedgehog, which encodes secreted signalling proteins, were also isolated as Deformed loss-of-function enhancers. Hedgehog mutant alleles also suppress the Polycomb phenotype. Mutations were also isolated in a few genes that interact with Deformed but not with Polycomb, indicating that the screen identified genes that are not general homeotic activators. Twoof these genes, cap ‘n’collarand defaced, have defects in embryonic head development that are similar to defects seen in loss of functionDefmed mutants. OMEOTIC proteinsencoded in the Anten- in embryos, and some evidence exists to support this H napedia and bithorax complexes of Drosophila, view.
    [Show full text]
  • The Evolution of Function in the Rab Family of Small Gtpases
    The Evolution of Function in the Rab Family of small GTPases Yoan Diekmann Dissertation presented to obtain the Ph.D. degree in Computational Biology Instituto de Tecnologia Química e Biológica | Universidade Nova de Lisboa Research work coordinated by: Oeiras, April, 2014 Cover: “The Rab Universe”. A circular version of Figure 2.5. The Evolution of Function in the Rab Family of small GTPases Yoan Diekmann, Computational Genomics Laboratory, Instituto Gulben- kian de Ciˆencia Declara¸c˜ao: Esta disserta¸c˜ao´eo resultado do meu pr´opriodesenvolvido entre Outubro de 2009 e Outubro de 2013 no laborat´oriodo Jos´eB. Pereira-Leal, PhD, Instituto Gulbenkian de Ciˆeciaem Oeiras, Portugal, no ˆambito do Programa de Doutoramento em Biologia Computacional (edi¸c˜ao2008-2009). Apoio financeiro: Apoio financeiro da FCT e do FSE no ˆambito do Quadro Comunit´ariode Apoio, bolsa de doutoramento SFRH/BD/33860/2009 e projectos HMSP-CT/SAU-ICT/0075/2009 e PCDC/EBB-BIO/119006/2010. Acknowledgements “Alors que vous achevez la lecture de mon expos´e,il est n´ecessaire de souligner le fait que ce que j’en ai retir´eest bien plus cons´equent.” Mit diesen Worten, die ich meinem Freund Axel schulde, begann was in der vorliegenden Arbeit seinen vorl¨aufigenH¨ohepunktfindet. So wahr wie damals ist der Satz auch heute, und das verdanke ich einer Reihe von Men- schen welche unerw¨ahnt zu lassen unm¨oglich ist. Obwohl das Schreiben die folgenden Namen notwendigerweise in eine Reihenfolge zw¨angt,so geb¨uhrt doch allen ihr g¨anzlich eigener Dank. Ich lasse der M¨udigkeit freien Lauf und schreibe einfach drauf los.
    [Show full text]
  • Scientific American Paper
    The Molecular Architects of Body Design Putting a human gene into a fly may sound like the basis for a science fiction film, but it demonstrates that nearly identical molecular mechanisms define body shapes in all animals by William McGinnis and Michael Kuziora ll animals develop from a single tems that mold our form, we humans Antennapedia adults are rare excep- fertilized egg cell that goes may be much more similar to our far tions, because most mutations in ho- A through many rounds of divi- distant worm and insect relatives than meotic genes cause fatal birth defects sion, often yielding millions of embry- we might like to think. So similar, in in Drosophila. Nevertheless, even those onic cells. In a dazzling and still myste- fact, thatÑas our work has shownÑcu- dying embryos can be quite instructive. rious feat of self-organization, these rious experimenters can use some hu- For instance, Ernesto Sanchez-Herrero cells arrange themselves into a com- man and mouse Hox genes to guide the and Gines Morata of the Independent plete organism, in which bone, muscle, development of fruit-ßy embryos. University of Madrid found that elimi- brain and skin integrate into a harmo- The story of these universal molecu- nation of three genes in the bithorax nious whole. The fundamental process lar architects actually begins with the complexÑUltrabithorax, abdominal-A is constant, but the results are not: hu- pioneering genetic studies of Edward and Abdominal-BÑis lethal. Yet such mans, mice, ßies and worms represent B. Lewis of the California Institute of mutant embryos survive long enough a wide range of body designs.
    [Show full text]
  • Information Processing in Biology: a Study on Signaling and Emergent
    Information processing in biology A study on signaling and emergent computation Tiago Ramalho M¨unchen2015 Information processing in biology A study on signaling and emergent computation Tiago Ramalho Dissertation an der Fakult¨atf¨urPhysik der Ludwig{Maximilians{Universit¨at M¨unchen vorgelegt von Tiago Ramalho aus Lissabon M¨unchen, den 10. Juni Erstgutachter: Prof. Dr. Ulrich Gerland Zweitgutachter: Prof. Dr. Erwin Frey Datum der müdlichen Prüfung: 23.10.2015 Zusammenfassung Erfolgreiche Organismen mussen¨ auf eine Vielzahl von Herausforderungen einer dynami- schen und unsicheren Umgebung angemessen reagieren. Die Grundmechanismen eines sol- chen Verhalten k¨onnen im Allgemeinen als Ein-/Ausgabeeinheiten beschrieben werden. Diese Einheiten bilden die Umweltbedingungen (Eing¨ange) auf assoziierte Reaktionen (Ausg¨ange) ab. Vor diesem Hintergrund ist es interessant zu versuchen diese Systeme mit Informationstheorie { eine Theorie entwickelt um mathematisch Ein-/Ausgabesysteme zu beschreiben { zu modellieren. Aus der Informationstheoretischen Sicht ist das Verhalten eines Organismus vom seinem Repertoire an m¨glichen Reaktionen unter verschiedenen Umgebungsbedingungen vollst¨andig charakterisiert. Unter dem Gesichtspunkt der naturlichen¨ Auslese ist es berechtigt anzu- nehmen, dass diese Ein-/Ausgabeabbildung zur Optimierung der Fitness des Organismus optimiert worden ist. Unter dieser Annahme, sollte es m¨oglich sein die mechanistischen De- tails der Implementierung zu abstrahieren und die zu Fitness fuhrenden¨ Grundprinzipien unter bestimmten Umweltbedingungen zu verstehen. Diese k¨onnen dann benutzt werden um Hypothesen uber¨ die zugrunde liegende Implementierung des Systems zu formulieren sowie um neuartige Reaktionen unter ¨außeren St¨orungen vorherzusagen. In dieser Arbeit wende ich Informationstheorie auf die Frage an, wie biologische Systeme komplexe Ausgaben mit relativ einfachen Mechanismen in einer robusten Weise erzeugen.
    [Show full text]
  • DEAF-1 Function Is Essential for the Early Embryonic Development Of
    ©2002Wiley-Liss,Inc. genesis33:67–76(2002) ARTICLE DEAF-1FunctionIsEssentialfortheEarlyEmbryonic DevelopmentofDrosophila AlexeyVeraksa,1†JamesKennison,2 andWilliamMcGinnis1* 1DivisionofBiology,UniversityofCalifornia,SanDiego,LaJolla,California 2LaboratoryofMolecularGenetics,NationalInstitutesofHealth,Bethesda,Maryland Received8February2002;Accepted19March2002 Summary:TheDrosophilaproteinDEAF-1isase- coreofaminoacidresiduesinDEAF-1andotherproteins quence-specificDNAbindingproteinthatwasisolated (GrossandMcGinnis,1995).NUDR(nuclearDEAF-1- asaputativecofactoroftheHoxproteinDeformed(Dfd). relatedfactor,alsoknownasSuppressinormDEAF-1)is Inthisstudy,weanalyzetheeffectsoflossorgainof anapparentmammalianorthologofDEAF-1andisthe DEAF-1functiononDrosophiladevelopment.Maternal/ zygoticmutationsofDEAF-1largelyresultinearlyem- onlynon-DrosophilaproteincontainingboththeSAND bryonicarrestpriortotheexpressionofzygoticseg- andthecarboxy-terminalMYNDdomain(Huggenviket mentationgenes,althoughafewembryosdevelopinto al.,1998;LeBoeufetal.,1998;Sugiharaetal.,1998; larvaewithsegmentationdefectsofvariableseverity. Michelsonetal.,1999;Bottomleyetal.,2001).NUDR OverexpressionofDEAF-1proteininembryoscanin- wascharacterizedasanuclearDNAbindingproteinthat ducedefectsinmigration/closureofthedorsalepider- alsopreferentiallybindsDNAsitescontainingTTCGmo- mis,andoverexpressioninadultprimordiacanstrongly tifs,withapreferenceforclusteredTTCGsequences. disruptthedevelopmentofeyeorwing.TheDEAF-1 ExperimentsonNUDRsuggestthatitisrequiredto proteinassociateswithmanydiscretesitesonpolytene
    [Show full text]
  • A Comparison of Deformed-Responsive Elements
    Copyright 2000 by the Genetics Society of America Regulation by Homeoproteins: A Comparison of Deformed-Responsive Elements Jeffrey A. Pederson,*,1 James W. LaFollette,* Cornelius Gross,²,2 Alexey Veraksa,² William McGinnis² and James W. Mahaffey* *Department of Genetics, North Carolina State University, Raleigh, North Carolina 27695-7614 and ²Department of Biology, University of California, San Diego, California 92093 Manuscript received March 8, 2000 Accepted for publication June 1, 2000 ABSTRACT Homeotic genes of Drosophila melanogaster encode transcription factors that specify segment identity by activating the appropriate set of target genes required to produce segment-speci®c characteristics. Advances in understanding target gene selection have been hampered by the lack of genes known to be directly regulated by the HOM-C proteins. Here we present evidence that the gene 1.28 is likely to be a direct target of Deformed in the maxillary segment. We identi®ed a 664-bp Deformed Response Element (1.28 DRE) that directs maxillary-speci®c expression of a reporter gene in transgenic embryos. The 1.28 DRE contains in vitro binding sites for Deformed and DEAF-1. The Deformed binding sites do not have the consensus sequence for cooperative binding with the cofactor Extradenticle, and we do not detect coopera- tive binding to these sites, though we cannot rule out an independent role for Extradenticle. Removing the four Deformed binding sites renders the 1.28 DRE inactive in vivo, demonstrating that these sites are necessary for activation of this enhancer element, and supporting the proposition that 1.28 is activated by Deformed. We show that the DEAF-1 binding region is not required for enhancer function.
    [Show full text]
  • University of Cincinnati
    UNIVERSITY OF CINCINNATI Date: 14-May-2010 I, Lindsay R Craig , hereby submit this original work as part of the requirements for the degree of: Doctor of Philosophy in Philosophy It is entitled: Scientific Change in Evolutionary Biology: Evo-Devo and the Developmental Synthesis Student Signature: Lindsay R Craig This work and its defense approved by: Committee Chair: Robert Skipper, PhD Robert Skipper, PhD 6/6/2010 690 Scientific Change in Evolutionary Biology: Evo-Devo and the Developmental Synthesis A dissertation submitted to the Graduate School of the University of Cincinnati in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Philosophy of the College of Arts and Sciences by Lindsay R. Craig B.A. Butler University M.A. University of Cincinnati May 2010 Advisory Committee: Associate Professor Robert Skipper, Jr., Chair/Advisor Professor Emeritus Richard M. Burian Assistant Professor Koffi N. Maglo Professor Robert C. Richardson Abstract Although the current episode of scientific change in the study of evolution, the Developmental Synthesis as I will call it, has attracted the attention of several philosophers, historians, and biologists, important questions regarding the motivation for and structure of the new synthesis are currently unanswered. The thesis of this dissertation is that the Developmental Synthesis is a two-phase multi-field integration motivated by the lack of adequate causal explanations of the origin of novel morphologies and the evolution of developmental processes over geologic time. I argue that the first phase of the Developmental Synthesis is a partial explanatory reconciliation. More specifically, I contend that the rise of the developmental gene concept and the discovery of highly conserved developmental genes helped demonstrate the overlap in explanatory interests between the developmental sciences and other scientific fields within the domain of evolutionary biology.
    [Show full text]
  • The Genome of the Choanoflagellate Monosiga Brevicollis and the Origins of Metazoan Multicellularity
    The genome of the choanoflagellate Monosiga brevicollis and the origins of metazoan multicellularity Nicole King 1,2 , M. Jody Westbrook 1* , Susan L. Young 1* , Alan Kuo 3, Monika Abedin 1, Jarrod Chapman 1, Stephen Fairclough 1, Uffe Hellsten 3, Yoh Isogai 1, Ivica Letunic 4, Michael Marr 5, David Pincus 6, Nicholas Putnam 1, Antonis Rokas 7, Kevin J. Wright 1, Richard Zuzow 1, William Dirks 1, Matthew Good 6, David Goodstein 1, Derek Lemons 8, Wanqing Li 9, Jessica Lyons 1, Andrea Morris 10 , Scott Nichols 1, Daniel J. Richter 1, Asaf Salamov 3, JGI Sequencing 3, Peer Bork 4, Wendell A. Lim 6, Gerard Manning 11 , W. Todd Miller 9, William McGinnis 8, Harris Shapiro 3, Robert Tjian 1, Igor V. Grigoriev 3, Daniel Rokhsar 1,3 1Department of Molecular and Cell Biology and the Center for Integrative Genomics, University of California, Berkeley, CA 94720, USA 2Department of Integrative Biology, University of California, Berkeley, CA 94720, USA 3Department of Energy Joint Genome Institute, Walnut Creek, CA 94598, USA 4EMBL, Meyerhofstrasse 1, 69012 Heidelberg, Germany 5Department of Biology, Brandeis University, Waltham, MA 02454 6Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA 7Vanderbilt University, Department of Biological Sciences, Nashville, TN 37235, USA 8Division of Biological Sciences, University of California, San Diego La Jolla, CA 92093 9Department of Physiology and Biophysics, Stony Brook University, Stony Brook, NY 11794 10 University of Michigan, Department of Cellular and Molecular Biology, Ann Arbor MI 48109 11 Razavi Newman Bioinformatics Center, Salk Institute for Biological Studies, La Jolla, CA 92037 *These authors contributed equally to this work.
    [Show full text]
  • Proquest Dissertations
    EVOLUTIONARY GENOMICS FROM ONTOGENY TO PHYLOGENY By CARLO G. ARTIERI, B.Sc., M.Sc. A Thesis Submitted to the School of Graduate Studies in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy McMaster University Copyright by Carlo Artieri, June 2009 Library and Archives Bibliothéque et 1*1 Canada Archives Canada Published Heritage Direction du Branch Patrimoine de Tédition 395 Wellington Street 395, rue Wellington Ottawa ON K1A 0N4 Ottawa ON K1A 0N4 Canada Canada Yourfile Votra reference ISBN: 978-0-494-62553-8 Ourfile Notre reference ISBN: 978-0-494-62553-8 NOTICE: AVIS: The author has granted a non- Uauteur a accordé une licence non exclusive exclusive license allowing Library and permettant å la Bibliothéque et Archives Archives Canada to reproduce, Canada de reproduire, publier, archiver, publish, archive, preserve, conserve, sauvegarder, conserver, transmettre au public communicate to the public by par telecommunication ou par Clnternet, préter, telecommunication or on the Internet, distribuer et vendre des theses partout dans le loan, distribute and seil theses monde, å des fins commerciales ou autres, sur worldwide, for commercial or non- support microforme, papier, électronique et/ou commercial purposes, in microform, autres formats. paper, electronic and/or any other formats. The author retains copyright L'auteur conserve la propriété du droit d'auteur ownership and moral rights in this et des droits moraux qui protege ætte thése. Ni thesis. Neither the thesis nor la thése ni des extraits substantiels de celle-ci substantial extracts from it may be ne doivent étre imprimés ou autrement printed or otherwise reproduced reproduits sans son autorisation.
    [Show full text]
  • Evidence for Positive and Negative Regulation of the Hox-3.1 Gene CHARLES J
    Proc. Nadl. Acad. Sci. USA Vol. 87, pp. 8462-8466, November 1990 Genetics Evidence for positive and negative regulation of the Hox-3.1 gene CHARLES J. BIEBERICH*t, MANUEL F. UTSETt, ALEXANDER AWGULEWITSCH§, AND FRANK H. RUDDLE*t Departments of *Biology and *Human Genetics, Yale University, P.O. Box 6666, New Haven, CT 06511; and §Department of Biochemistry and Molecular Biology, Medical University of South Carolina, 171 Ashley Avenue, Charleston, SC 29425 Contributed by Frank H. Ruddle, July 23, 1990 ABSTRACT The region-specific patterns of expression of gene more 5' within the same cluster (6-10). Furthermore, it mouse homeobox genes are considered important for estab- appears that for at least some of the Hox genes, most notably lishing the embryonic body plan. A 5-kilobase (kb) DNA Hox-3.1 and Hox-2.5, the region-specific expression patterns fragment from the Hox-3.1 locus that is sufficient to confer are dynamic, showing two distinct phases: an "early" pos- region-specific expression to a (3-galactosidase reporter gene in terior pattern at 8.5 and 9.5 days postcoitum (p.c.) and a transgenic mouse embryos has been defined. The observed "late" more anterior pattern with altered dorsoventral local- reporter gene expression pattern closely parallels endogenous ization within the neural tube at 10.5 days p.c. and later (11, Hox-3.1 expression in 8- to 9.5-day postcoitum (p.c.) embryos. 12). While the anterior shift could result from increased At 10.5 days p.c. and later, the pattern of X3-galactosidase growth in the neural tube relative to the rest of the embryo, activity diverges from the Hox-3.1 pattern, and an inappro- the dorsoventral localization for each gene represents a new priately high level of reporter gene expression is observed in cellular specificity.
    [Show full text]