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Relaxed Selection in the Wild
TREE-1109; No of Pages 10 Review Relaxed selection in the wild David C. Lahti1, Norman A. Johnson2, Beverly C. Ajie3, Sarah P. Otto4, Andrew P. Hendry5, Daniel T. Blumstein6, Richard G. Coss7, Kathleen Donohue8 and Susan A. Foster9 1 Department of Biology, University of Massachusetts, Amherst, MA 01003, USA 2 Department of Plant, Soil, and Insect Sciences, University of Massachusetts, Amherst, MA 01003, USA 3 Center for Population Biology, University of California, Davis, CA 95616, USA 4 Department of Zoology, University of British Columbia, Vancouver, BC V6T 1Z4, Canada 5 Redpath Museum and Department of Biology, McGill University, Montreal, QC H3A 2K6, Canada 6 Department of Ecology and Evolutionary Biology, University of California, Los Angeles, CA 90095, USA 7 Department of Psychology, University of California, Davis, CA 95616, USA 8 Department of Biology, Duke University, Durham, NC 02138, USA 9 Department of Biology, Clark University, Worcester, MA 01610, USA Natural populations often experience the weakening or are often less clear than typical cases of trait evolution. removal of a source of selection that had been important When an environmental change results in strong selection in the maintenance of one or more traits. Here we refer to on a trait from a known source, a prediction for trait these situations as ‘relaxed selection,’ and review recent evolution often follows directly from this fact [2]. When studies that explore the effects of such changes on traits such a strong source of selection is removed, however, no in their ecological contexts. In a few systems, such as the clear prediction emerges. Rather, the likelihood of various loss of armor in stickleback, the genetic, developmental consequences can only be understood by integrating the and ecological bases of trait evolution are being discov- remaining sources of selection and processes at all levels of ered. -
Inclusive Fitness As a Criterion for Improvement LSE Research Online URL for This Paper: Version: Accepted Version
Inclusive fitness as a criterion for improvement LSE Research Online URL for this paper: http://eprints.lse.ac.uk/104110/ Version: Accepted Version Article: Birch, Jonathan (2019) Inclusive fitness as a criterion for improvement. Studies in History and Philosophy of Science Part C :Studies in History and Philosophy of Biological and Biomedical Sciences, 76. ISSN 1369-8486 https://doi.org/10.1016/j.shpsc.2019.101186 Reuse This article is distributed under the terms of the Creative Commons Attribution- NonCommercial-NoDerivs (CC BY-NC-ND) licence. This licence only allows you to download this work and share it with others as long as you credit the authors, but you can’t change the article in any way or use it commercially. More information and the full terms of the licence here: https://creativecommons.org/licenses/ [email protected] https://eprints.lse.ac.uk/ Inclusive Fitness as a Criterion for Improvement Jonathan Birch Department of Philosophy, Logic and Scientific Method, London School of Economics and Political Science, London, WC2A 2AE, United Kingdom. Email: [email protected] Webpage: http://personal.lse.ac.uk/birchj1 This article appears in a special issue of Studies in History & Philosophy of Biological & Biomedical Sciences on Optimality and Adaptation in Evolutionary Biology, edited by Nicola Bertoldi. 16 July 2019 1 Abstract: I distinguish two roles for a fitness concept in the context of explaining cumulative adaptive evolution: fitness as a predictor of gene frequency change, and fitness as a criterion for phenotypic improvement. Critics of inclusive fitness argue, correctly, that it is not an ideal fitness concept for the purpose of predicting gene- frequency change, since it relies on assumptions about the causal structure of social interaction that are unlikely to be exactly true in real populations, and that hold as approximations only given a specific type of weak selection. -
Doxorubicin-Induced Death in Neuroblastoma Does Not Involve Death Receptors in S-Type Cells and Is Caspase-Independent in N-Type Cells
Oncogene (2002) 21, 6132 – 6137 ª 2002 Nature Publishing Group All rights reserved 0950 – 9232/02 $25.00 www.nature.com/onc Doxorubicin-induced death in neuroblastoma does not involve death receptors in S-type cells and is caspase-independent in N-type cells Sally Hopkins-Donaldson1, Pu Yan1, Katia Balmas Bourloud1, Annick Muhlethaler1, Jean-Luc Bodmer2 and Nicole Gross*,1 1Department of Pediatric Onco-Hematology, Centre Hospitalier Universitaire Vaudois, CH1011 Lausanne, Switzerland; 2Institute of Biochemistry, University of Lausanne, CH-1066, Epalinges, Switzerland Death induced by doxorubicin (dox) in neuroblastoma tumors in infants frequently undergo spontaneous (NB) cells was originally thought to occur via the Fas remission. Failure to undergo programmed cell death pathway, however since studies suggest that caspase-8 is a putative mechanism for cancer cell resistance to expression is silenced in most high stage NB tumors, it is chemotherapy, while in contrast spontaneous remission more probable that dox-induced death occurs via a is thought to be a result of increased apoptosis (Oue et different mechanism. Caspase-8 silenced N-type invasive al., 1996). NB cell lines LAN-1 and IMR-32 were investigated for Apoptosis signaling occurs via two different path- their sensitivity to dox, and compared to S-type ways which converge on a common machinery of cell noninvasive SH-EP NB cells expressing caspase-8. All demise that is activated by caspases (Strasser et al., cell lines had similar sensitivities to dox, independently of 2000). The death receptor pathway is activated by caspase-8 expression. Dox induced caspase-3, -7, -8 and ligands of the tumor necrosis factor (TNF) family -9 and Bid cleavage in S-type cells and death was which induce the trimerization of their cognate blocked by caspase inhibitors but not by oxygen radical receptors (Daniel et al., 2001). -
Drosophila Melanogaster”
| PRIMER More than Meets the Eye: A Primer for “Timing of Locomotor Recovery from Anoxia Modulated by the white Gene in Drosophila melanogaster” Bradley M. Hersh1 Department of Biology, Allegheny College, Meadville, Pennsylvania 16335 ORCID ID: 0000-0003-2098-4417 (B.M.H.) SUMMARY A single gene might have several functions within an organism, and so mutational loss of that gene has multiple effects across different physiological systems in the organism. Though the white gene in Drosophila melanogaster was identified originally for its effect on fly eye color, an article by Xiao and Robertson in the June 2016 issue of GENETICS describes a function for the white gene in the response of Drosophila to oxygen deprivation. This Primer article provides background information on the white gene, the phenomenon of pleiotropy, and the molecular and genetic approaches used in the study to demonstrate a new behavioral function for the white gene. KEYWORDS education; Drosophila; pleiotropy; behavior TABLE OF CONTENTS Abstract 1369 Molecular Nature of the white Gene 1370 The Challenge of Pleiotropy 1370 Tissue-Specific Expression and RNA Interference (RNAi) 1371 Understanding the Experimental Details 1372 Establishing a behavioral phenotype 1372 Introgression: eliminating the trivial 1372 Dosage and position effect: complicating the story 1373 Molecular tricks: dissecting function and location of action 1373 Suggestions for Classroom Use 1374 Questions for Discussion 1374 HE white gene was the first Drosophila melanogaster the first attached-X and ring-X chromosome variants), is re- Tmutant discovered by Thomas Hunt Morgan in 1910, ported to have exclaimed “Oh, I do hope the white-eyed flyis following an exhaustive search for variant forms of the fly still alive” from her hospital bed after having just delivered (Morgan 1910). -
123 Author's Personal Copy
Author's personal copy Synthese DOI 10.1007/s11229-012-0147-2 Models of data and theoretical hypotheses: a case-study in classical genetics Marion Vorms Received: 17 July 2011 / Accepted: 13 October 2011 © Springer Science+Business Media B.V. 2012 Abstract Linkage (or genetic) maps are graphs, which are intended to represent the linear ordering of genes on the chromosomes. They are constructed on the basis of statistical data concerning the transmission of genes. The invention of this technique in 1913 was driven by Morgan’s group’s adoption of a set of hypotheses concerning the physical mechanism of heredity. These hypotheses were themselves grounded in Morgan’s defense of the chromosome theory of heredity, according to which chro- mosomes are the physical basis of genes. In this paper, I analyze the 1919 debate between William Castle and Morgan’s group, about the construction of genetic maps. The official issue of the debate concerns the arrangement of genes on chromosomes. However, the disputants tend to carry out the discussions about how one should model the data in order to draw predictions concerning the transmission of genes; the debate does not bear on the data themselves, nor does it focus on the hypotheses explaining these data. The main criteria that are appealed to by the protagonists are simplicity and predictive efficacy. However, I show that both parties’ assessments of the simplicity and predictive efficacy of different ways of modeling the data themselves depend on background theoretical positions. I aim at clarifying how preference for a given model and theoretical commitments articulate. -
Genetically Modified Mosquitoes Educator Materials
Genetically Modified Mosquitoes Scientists at Work Educator Materials OVERVIEW This document provides background information, discussion questions, and responses that complement the short video “Genetically Modified Mosquitoes” from the Scientists at Work series. The Scientists at Work series is intended to provide insights into the daily work of scientists that builds toward discoveries. The series focuses especially on scientists in the field and what motivates their work. This 8-minute 35-second video is appropriate for any life science student audience. It can be used as a review of the nature of science or to enhance a discussion on transgenic technology. Classroom implementation of the material in this document might include assigning select discussion questions to small groups of students or selecting the top five questions to discuss as a class. KEY CONCEPTS • Researchers genetically modified mosquitoes to help prevent the spread of a virus. • Male GM mosquitoes pass on a lethality gene to the offspring when they mate with non-GM females in the wild. CURRICULUM CONNECTIONS Standards Curriculum Connection NGSS (2013) HS-LS1.A, HS-LS3.A AP Bio (2015) 3.A.1 IB Bio (2016) 3.1, 3.5 Vision and Change (2009) CC1, CC2, CC3 PRIOR KNOWLEDGE Students should • be familiar with the idea that genes code for proteins and that genetic information can be passed to offspring. • have some understanding of transgenic technology and what it means for an organism to be genetically modified. BACKGROUND INFORMATION Mosquitoes can transmit pathogens that cause many human diseases, such as malaria, yellow fever, dengue fever, chikungunya, and Zika fever. -
Transgenic Rescue from Embryonic Lethality and Renal Carcinogenesis in the Eker Rat Model by Introduction of a Wild-Type Tsc2 Ge
Proc. Natl. Acad. Sci. USA Vol. 94, pp. 3990–3993, April 1997 Medical Sciences Transgenic rescue from embryonic lethality and renal carcinogenesis in the Eker rat model by introduction of a wild-type Tsc2 gene (hereditary cancerytwo-hit modelytumor suppressor geneyanimal modelygene therapy) TOSHIYUKI KOBAYASHI*, HIROAKI MITANI*, RI-ICHI TAKAHASHI†,MASUMI HIRABAYASHI†,MASATSUGU UEDA†, HIROSHI TAMURA‡, AND OKIO HINO*§ *Department of Experimental Pathology, Cancer Institute, 1-37-1 Kami-Ikebukuro, Toshima-ku, Tokyo 170, Japan; †YS New Technology Institute Inc., Shimotsuga-gun, Tochigi 329-05, Japan; and ‡Laboratory of Animal Center, Teikyo University School of Medicine, 2-11-1, Kaga, Itabashi-ku, Tokyo 173, Japan Communicated by Takashi Sugimura, National Cancer Center, Tokyo, Japan, February 3, 1997 (received for review December 9, 1996) ABSTRACT We recently reported that a germ-line inser- activity for Rap1a and localizes to Golgi apparatus. Other tion in the rat homologue of the human tuberous sclerosis gene potential functional domains include two transcriptional acti- (TSC2) gives rise to dominantly inherited cancer in the Eker vation domains (AD1 and AD2) in the carboxyl terminus of the rat model. In this study, we constructed transgenic Eker rats Tsc2 gene product (19), a zinc-finger-like region (our unpub- with introduction of a wild-type Tsc2 gene to ascertain lished observation), and a potential src-homology 3 region whether suppression of the Eker phenotype is possible. Rescue (SH3) binding domain (20). However, the function of tuberin from embryonic lethality of mutant homozygotes (EkeryEker) is not yet fully understood. and suppression of N-ethyl-N-nitrosourea-induced renal car- Human tuberous sclerosis is an autosomal dominant genetic cinogenesis in heterozygotes (Ekery1) were both observed, disease characterized by phacomatosis with manifestations defining the germ-line Tsc2 mutation in the Eker rat as that include mental retardation, seizures, and angiofibroma, embryonal lethal and tumor predisposing mutation. -
I Xio- and Made the Rather Curious Assumption That the Mutant Is
NOTES AND COMMENTS NATURAL SELECTION AND THE EVOLUTION OF DOMINANCE P. M. SHEPPARD Deportment of Genetics, University of Liverpool and E.B. FORD Genetic Laboratories, Department of Zoology, Oxford 1. INTRODUCTION CROSBY(i 963) criticises the hypothesis that dominance (or recessiveness) has evolved and is not an attribute of the allelomorph when it arose for the first time by mutation. None of his criticisms is new and all have been discussed many times. However, because of a number of apparent mis- understandings both in previous discussions and in Crosby's paper, and the fact that he does not refer to some important arguments opposed to his own view, it seems necessary to reiterate some of the previous discussion. Crosby's criticisms fall into two parts. Firstly, he maintains, as did Wright (1929a, b) and Haldane (1930), that the selective advantage of genes modifying dominance, being of the same order of magnitude as the mutation rate, is too small to have any evolutionary effect. Secondly, he criticises, as did Wright (5934), the basic assumption that a new mutation when it first arises produces a phenotype somewhat intermediate between those of the two homozygotes. 2.THE SELECTION COEFFICIENT INVOLVED IN THE EVOLUTION OF DOMINANCE Thereis no doubt that the selective advantage of modifiers of dominance is of the order of magnitude of the mutation rate of the gene being modified. Crosby (p. 38) considered a hypothetical example with a mutation rate of i xio-and made the rather curious assumption that the mutant is dominant in the absence of modifiers of dominance. -
Calvin Bridges' Experiments on Nondisjunction As Evidence for The
Published on The Embryo Project Encyclopedia (https://embryo.asu.edu) Calvin Bridges’ Experiments on Nondisjunction as Evidence for the Chromosome Theory of Heredity (1913-1916) [1] By: Gleason, Kevin Keywords: Thomas Hunt Morgan [2] Drosophila [3] From 1913 to 1916, Calvin Bridges performed experiments that indicatedg enes [5] are found on chromosomes. His experiments were a part of his doctoral thesis advised by Thomas Hunt Morgan [6] in New York, New York. In his experiments, Bridges studied Drosophila [7], the common fruit fly, and by doing so showed that a process called nondisjunction caused chromosomes, under some circumstances, to fail to separate when forming sperm [8] and egg [9] cells. Nondisjunction, as described by Bridges, caused sperm [8] or egg [9] cells to contain abnormal amounts of chromosomes. In some cases, that caused the offspring produced by the sperm [8] or eggs to display traits that they would typically not have. His research on nondisjunction provided evidence that chromosomes carry genetic traits, including those that determine the sex of an organism. At the beginning of the twentieth century, other researchers were starting to establish the role that chromosomes play in heredity. In 1910, Morgan provided some evidence that genes [5], or the material factors that were thought to control heredity, are located on the chromosome. While Morgan was mating Drosophila [10], which typically had red eyes, Morgan found that one of the offspring flies had white eyes. He proceeded to mate the white-eyed fly with other flies, and he observed a generation of offspring in which only some of the male offspring, but only the male offspring, had white eyes. -
Alfred Henry Sturtevant (1891–1970) [1]
Published on The Embryo Project Encyclopedia (https://embryo.asu.edu) Alfred Henry Sturtevant (1891–1970) [1] By: Gleason, Kevin Keywords: Thomas Hunt Morgan [2] Drosophila [3] Alfred Henry Sturtevant studied heredity in fruit flies in the US throughout the twentieth century. From 1910 to 1928, Sturtevant worked in Thomas Hunt Morgan’s research lab in New York City, New York. Sturtevant, Morgan, and other researchers established that chromosomes play a role in the inheritance of traits. In 1913, as an undergraduate, Sturtevant created one of the earliest genetic maps of a fruit fly chromosome, which showed the relative positions of genes [4] along the chromosome. At the California Institute of Technology [5] in Pasadena, California, he later created one of the firstf ate maps [6], which tracks embryonic cells throughout their development into an adult organism. Sturtevant’s contributions helped scientists explain genetic and cellular processes that affect early organismal development. Sturtevant was born 21 November 1891 in Jacksonville, Illinois, to Harriet Evelyn Morse and Alfred Henry Sturtevant. Sturtevant was the youngest of six children. During Sturtevant’s early childhood, his father taught mathematics at Illinois College in Jacksonville. However, his father left that job to pursue farming, eventually relocating seven-year-old Sturtevant and his family to Mobile, Alabama. In Mobile, Sturtevant attended a single room schoolhouse until he entered a public high school. In 1908, Sturtevant entered Columbia University [7] in New York City, New York. As a sophomore, Sturtevant took an introductory biology course taught by Morgan, who was researching how organisms transfer observable characteristics, such as eye color, to their offspring. -
Using Drosophila to Teach Genetics
Curriculum Units by Fellows of the Yale-New Haven Teachers Institute 1996 Volume V: Genetics in the 21st Century: Destiny, Chance or Choice Using Drosophila to Teach Genetics Curriculum Unit 96.05.01 by Christin E. Arnini The objectives of this unit are to take basic concepts of genetics and apply them to an organism, easily raised and observed in the classroom. It has been a challenge in the teaching of High School Biology, to take the abstract ideas of genes, chromosomes, heredity, and make them visable and tangible for the students. Drosophila melanogaster offers a way for teachers to help students make connections between populations, the organism, the cell, the chromosome, the gene, and the DNA. As a part of a unit on genetics, this unit on Drosophila can give students the opportunity to get to know an organism well, observing closely its development and physical characteristics, and then questioning how it is that the fly came to be this way. Unit Format: I. Discussion of Drosophila 1. Review of genetics concepts 2. Thomas Hunt Morgan and the historical frame 3. Drosophila chromosomes, characteristics, and developmental stages 4. Mutations 5. Homeobox genes 6. Homologs in other vertebrates 7. Making a map 8. DNA Sequencing II. Activities: 1. Observations of the individual flies, 2. Doing genetic crossses, and predicting offspring outcomes in the Lab, 3. Salivary gland extraction, and staining of chromosomes 4. Creating a genetic map 5. DNA sequencing simulation, 6. Virtual Fly Lab. III. Appendix IV. Bibliography and resources Curriculum Unit 96.05.01 1 of 21 Chromosomes are the structures that contain the hereditary material of an organism. -
1 the Limits of Selection Under Plant Domestication Robin G Allaby1
The limits of selection under plant domestication Robin G Allaby1* ,Dorian Q Fuller2, James L Kitchen1, 3 1. School of Life Sciences, Gibbet Hill Campus, University of Warwick, Coventry CV4 7AL 2. Institute of Archaeology, University College London, 31-34 Gordon Square, London WC1H 0PY 3. Computational and Systems Biology, Rothamsted, Harpenden, Herts. * corresponding author email: [email protected] 1 Abstract Plant domestication involved a process of selection through human agency of a series of traits collectively termed the domestication syndrome. Current debate concerns the pace at which domesticated plants emerged from cultivated wild populations and how many genes were involved. Here we present simulations that test how many genes could have been involved by considering the cost of selection. We demonstrate the selection load that can be endured by populations increases with decreasing selection coefficients and greater numbers of loci down to values of about s = 0.005, causing a driving force that increases the number of loci under selection. As the number of loci under selection increases, an effect of co-selection increases resulting in individual unlinked loci being fixed more rapidly in out-crossing populations, representing a second driving force to increase the number of loci under selection. In inbreeding systems co-selection results in interference and reduced rates of fixation but does not reduce the size of the selection load that can be endured. These driving forces result in an optimum pace of genome evolution in which 50-100 loci are the most that could be under selection in a cultivation regime. Furthermore, the simulations do not preclude the existence of selective sweeps but demonstrate that they come at a cost of the selection load that can be endured and consequently a reduction of the capacity of plants to adapt to new environments, which may contribute to the explanation of why selective sweeps have been so rarely detected in genome studies.