Molecular Lamarckism: on the Evolution of Human Intelligence
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Heritability in the Era of Molecular Genetics: Some Thoughts for Understanding Genetic Influences on Behavioural Traits
European Journal of Personality, Eur. J. Pers. 25: 254–266 (2011) Published online (wileyonlinelibrary.com) DOI: 10.1002/per.836 Heritability in the Era of Molecular Genetics: Some Thoughts for Understanding Genetic Influences on Behavioural Traits WENDY JOHNSON1,2*, LARS PENKE1 and FRANK M. SPINATH3 1Centre for Cognitive Ageing and Cognitive Epidemiology and Department of Psychology, University of Edinburgh, Edinburgh, UK 2Department of Psychology, University of Minnesota, Minneapolis, Minnesota, USA 3Department of Psychology, Saarland University, Saarbruecken, Germany Abstract: Genetic influences on behavioural traits are ubiquitous. When behaviourism was the dominant paradigm in psychology, demonstrations of heritability of behavioural and psychological constructs provided important evidence of its limitations. Now that genetic influences on behavioural traits are generally accepted, we need to recognise the limitations of heritability as an indicator of both the aetiology and likelihood of discovering molecular genetic associations with behavioural traits. We review those limitations and conclude that quantitative genetics and genetically informative research designs are still critical to understanding the roles of gene‐environment interplay in developmental processes, though not necessarily in the ways commonly discussed. Copyright © 2011 John Wiley & Sons, Ltd. Key words: genetic influences; twin study; heritability Much is often made of new findings of the presence of environmental influences but emphasised that these genetic influences -
Population Size and the Rate of Evolution
Review Population size and the rate of evolution 1,2 1 3 Robert Lanfear , Hanna Kokko , and Adam Eyre-Walker 1 Ecology Evolution and Genetics, Research School of Biology, Australian National University, Canberra, ACT, Australia 2 National Evolutionary Synthesis Center, Durham, NC, USA 3 School of Life Sciences, University of Sussex, Brighton, UK Does evolution proceed faster in larger or smaller popu- mutations occur and the chance that each mutation lations? The relationship between effective population spreads to fixation. size (Ne) and the rate of evolution has consequences for The purpose of this review is to synthesize theoretical our ability to understand and interpret genomic varia- and empirical knowledge of the relationship between tion, and is central to many aspects of evolution and effective population size (Ne, Box 1) and the substitution ecology. Many factors affect the relationship between Ne rate, which we term the Ne–rate relationship (NeRR). A and the rate of evolution, and recent theoretical and positive NeRR implies faster evolution in larger popula- empirical studies have shown some surprising and tions relative to smaller ones, and a negative NeRR implies sometimes counterintuitive results. Some mechanisms the opposite (Figure 1A,B). Although Ne has long been tend to make the relationship positive, others negative, known to be one of the most important factors determining and they can act simultaneously. The relationship also the substitution rate [5–8], several novel predictions and depends on whether one is interested in the rate of observations have emerged in recent years, causing some neutral, adaptive, or deleterious evolution. Here, we reassessment of earlier theory and highlighting some gaps synthesize theoretical and empirical approaches to un- in our understanding. -
Transformations of Lamarckism Vienna Series in Theoretical Biology Gerd B
Transformations of Lamarckism Vienna Series in Theoretical Biology Gerd B. M ü ller, G ü nter P. Wagner, and Werner Callebaut, editors The Evolution of Cognition , edited by Cecilia Heyes and Ludwig Huber, 2000 Origination of Organismal Form: Beyond the Gene in Development and Evolutionary Biology , edited by Gerd B. M ü ller and Stuart A. Newman, 2003 Environment, Development, and Evolution: Toward a Synthesis , edited by Brian K. Hall, Roy D. Pearson, and Gerd B. M ü ller, 2004 Evolution of Communication Systems: A Comparative Approach , edited by D. Kimbrough Oller and Ulrike Griebel, 2004 Modularity: Understanding the Development and Evolution of Natural Complex Systems , edited by Werner Callebaut and Diego Rasskin-Gutman, 2005 Compositional Evolution: The Impact of Sex, Symbiosis, and Modularity on the Gradualist Framework of Evolution , by Richard A. Watson, 2006 Biological Emergences: Evolution by Natural Experiment , by Robert G. B. Reid, 2007 Modeling Biology: Structure, Behaviors, Evolution , edited by Manfred D. Laubichler and Gerd B. M ü ller, 2007 Evolution of Communicative Flexibility: Complexity, Creativity, and Adaptability in Human and Animal Communication , edited by Kimbrough D. Oller and Ulrike Griebel, 2008 Functions in Biological and Artifi cial Worlds: Comparative Philosophical Perspectives , edited by Ulrich Krohs and Peter Kroes, 2009 Cognitive Biology: Evolutionary and Developmental Perspectives on Mind, Brain, and Behavior , edited by Luca Tommasi, Mary A. Peterson, and Lynn Nadel, 2009 Innovation in Cultural Systems: Contributions from Evolutionary Anthropology , edited by Michael J. O ’ Brien and Stephen J. Shennan, 2010 The Major Transitions in Evolution Revisited , edited by Brett Calcott and Kim Sterelny, 2011 Transformations of Lamarckism: From Subtle Fluids to Molecular Biology , edited by Snait B. -
An Unusually Low Microsatellite Mutation Rate in Dictyostelium Discoideum,An Organism with Unusually Abundant Microsatellites
Copyright Ó 2007 by the Genetics Society of America DOI: 10.1534/genetics.107.076067 An Unusually Low Microsatellite Mutation Rate in Dictyostelium discoideum,an Organism With Unusually Abundant Microsatellites Ryan McConnell, Sara Middlemist, Clea Scala, Joan E. Strassmann and David C. Queller1 Department of Ecology and Evolutionary Biology, Rice University, Houston, Texas 77005 Manuscript received May 18, 2007 Accepted for publication September 4, 2007 ABSTRACT The genome of the social amoeba Dictyostelium discoideum is known to have a very high density of microsatellite repeats, including thousands of triplet microsatellite repeats in coding regions that apparently code for long runs of single amino acids. We used a mutation accumulation study to see if unusually high microsatellite mutation rates contribute to this pattern. There was a modest bias toward mutations that increase repeat number, but because upward mutations were smaller than downward ones, this did not lead to a net average increase in size. Longer microsatellites had higher mutation rates than shorter ones, but did not show greater directional bias. The most striking finding is that the overall mutation rate is the lowest reported for microsatellites: 1 3 10À6 for 10 dinucleotide loci and 6 3 10À6 for 52 trinucleotide loci (which were longer). High microsatellite mutation rates therefore do not explain the high incidence of microsatellites. The causal relation may in fact be reversed, with low mutation rates evolving to protect against deleterious fitness effects of mutation at the numerous microsatellites. ICROSATELLITES, also known as simple se- In humans, certain triplet repeats that occur in or M quence repeats, are long stretches of a short near coding regions are subject to expansions that (1–6 bp), tandemly repeated DNA unit, such as the directly cause genetic diseases (Ashley and Warren motif CAA repeated 20 times. -
High Heritability of Telomere Length, but Low Evolvability, and No Significant
bioRxiv preprint doi: https://doi.org/10.1101/2020.12.16.423128; this version posted December 16, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 High heritability of telomere length, but low evolvability, and no significant 2 heritability of telomere shortening in wild jackdaws 3 4 Christina Bauch1*, Jelle J. Boonekamp1,2, Peter Korsten3, Ellis Mulder1, Simon Verhulst1 5 6 Affiliations: 7 1 Groningen Institute for Evolutionary Life Sciences, University of Groningen, Nijenborgh 7, 8 9747AG Groningen, The Netherlands 9 2 present address: Institute of Biodiversity Animal Health & Comparative Medicine, College 10 of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, United 11 Kingdom 12 3 Department of Animal Behaviour, Bielefeld University, Morgenbreede 45, 33615 Bielefeld, 13 Germany 14 15 16 * Correspondence to: 17 [email protected] 18 19 Running head: High heritability of telomere length bioRxiv preprint doi: https://doi.org/10.1101/2020.12.16.423128; this version posted December 16, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 20 Abstract 21 Telomere length (TL) and shortening rate predict survival in many organisms. Evolutionary 22 dynamics of TL in response to survival selection depend on the presence of genetic variation 23 that selection can act upon. However, the amount of standing genetic variation is poorly known 24 for both TL and TL shortening rate, and has not been studied for both traits in combination in 25 a wild vertebrate. -
Adaptive Tuning of Mutation Rates Allows Fast Response to Lethal Stress In
Manuscript 1 Adaptive tuning of mutation rates allows fast response to lethal stress in 2 Escherichia coli 3 4 a a a a a,b 5 Toon Swings , Bram Van den Bergh , Sander Wuyts , Eline Oeyen , Karin Voordeckers , Kevin J. a,b a,c a a,* 6 Verstrepen , Maarten Fauvart , Natalie Verstraeten , Jan Michiels 7 8 a 9 Centre of Microbial and Plant Genetics, KU Leuven - University of Leuven, Kasteelpark Arenberg 20, 10 3001 Leuven, Belgium b 11 VIB Laboratory for Genetics and Genomics, Vlaams Instituut voor Biotechnologie (VIB) Bioincubator 12 Leuven, Gaston Geenslaan 1, 3001 Leuven, Belgium c 13 Smart Systems and Emerging Technologies Unit, imec, Kapeldreef 75, 3001 Leuven, Belgium * 14 To whom correspondence should be addressed: Jan Michiels, Department of Microbial and 2 15 Molecular Systems (M S), Centre of Microbial and Plant Genetics, Kasteelpark Arenberg 20, box 16 2460, 3001 Leuven, Belgium, [email protected], Tel: +32 16 32 96 84 1 Manuscript 17 Abstract 18 19 While specific mutations allow organisms to adapt to stressful environments, most changes in an 20 organism's DNA negatively impact fitness. The mutation rate is therefore strictly regulated and often 21 considered a slowly-evolving parameter. In contrast, we demonstrate an unexpected flexibility in 22 cellular mutation rates as a response to changes in selective pressure. We show that hypermutation 23 independently evolves when different Escherichia coli cultures adapt to high ethanol stress. 24 Furthermore, hypermutator states are transitory and repeatedly alternate with decreases in mutation 25 rate. Specifically, population mutation rates rise when cells experience higher stress and decline again 26 once cells are adapted. -
IN EVOLUTION JACK LESTER KING UNIVERSITY of CALIFORNIA, SANTA BARBARA This Paper Is Dedicated to Retiring University of California Professors Curt Stern and Everett R
THE ROLE OF MUTATION IN EVOLUTION JACK LESTER KING UNIVERSITY OF CALIFORNIA, SANTA BARBARA This paper is dedicated to retiring University of California Professors Curt Stern and Everett R. Dempster. 1. Introduction Eleven decades of thought and work by Darwinian and neo-Darwinian scientists have produced a sophisticated and detailed structure of evolutionary ,theory and observations. In recent years, new techniques in molecular biology have led to new observations that appear to challenge some of the basic theorems of classical evolutionary theory, precipitating the current crisis in evolutionary thought. Building on morphological and paleontological observations, genetic experimentation, logical arguments, and upon mathematical models requiring simplifying assumptions, neo-Darwinian theorists have been able to make some remarkable predictions, some of which, unfortunately, have proven to be inaccurate. Well-known examples are the prediction that most genes in natural populations must be monomorphic [34], and the calculation that a species could evolve at a maximum rate of the order of one allele substitution per 300 genera- tions [13]. It is now known that a large proportion of gene loci are polymorphic in most species [28], and that evolutionary genetic substitutions occur in the human line, for instance, at a rate of about 50 nucleotide changes per generation [20], [24], [25], [26]. The puzzling observation [21], [40], [46], that homologous proteins in different species evolve at nearly constant rates is very difficult to account for with classical evolutionary theory, and at the very least gives a solid indication that there are qualitative differences between the ways molecules evolve and the ways morphological structures evolve. -
Environment-Sensitive Epigenetics and the Heritability of Complex Diseases
INVESTIGATION Environment-Sensitive Epigenetics and the Heritability of Complex Diseases Robert E. Furrow,*,1 Freddy B. Christiansen,† and Marcus W. Feldman* *Department of Biology, Stanford University, Stanford, California 94305, and †Department of Bioscience and Bioinformatics Research Center, University of Aarhus, DK-8000 Aarhus C, Denmark ABSTRACT Genome-wide association studies have thus far failed to explain the observed heritability of complex human diseases. This is referred to as the “missing heritability” problem. However, these analyses have usually neglected to consider a role for epigenetic variation, which has been associated with many human diseases. We extend models of epigenetic inheritance to investigate whether environment-sensitive epigenetic modifications of DNA might explain observed patterns of familial aggregation. We find that variation in epigenetic state and environmental state can result in highly heritable phenotypes through a combination of epigenetic and environmental inheritance. These two inheritance processes together can produce familial covariances significantly higher than those predicted by models of purely epigenetic inheritance and similar to those expected from genetic effects. The results suggest that epigenetic variation, inherited both directly and through shared environmental effects, may make a key contribution to the missing heritability. HE challenges of identifying the common or rare genes a change in DNA sequence. Such modifications include Tthat contribute to the transmission of heritable human methylation of cytosine nucleotides at CpG sites and histone diseases and other complex phenotypes have been discussed protein modification. Such epigenetic modifications may be for some time (Moran 1973; Layzer 1974; Feldman and transmissible across generations or arise de novo each gen- Lewontin 1975; Kamin and Goldberger 2002). -
Metazoan Ribosome Inactivating Protein Encoding Genes Acquired by Horizontal Gene Transfer Received: 30 September 2016 Walter J
www.nature.com/scientificreports OPEN Metazoan Ribosome Inactivating Protein encoding genes acquired by Horizontal Gene Transfer Received: 30 September 2016 Walter J. Lapadula1, Paula L. Marcet2, María L. Mascotti1, M. Virginia Sanchez-Puerta3 & Accepted: 5 April 2017 Maximiliano Juri Ayub1 Published: xx xx xxxx Ribosome inactivating proteins (RIPs) are RNA N-glycosidases that depurinate a specific adenine residue in the conserved sarcin/ricin loop of 28S rRNA. These enzymes are widely distributed among plants and their presence has also been confirmed in several bacterial species. Recently, we reported for the first timein silico evidence of RIP encoding genes in metazoans, in two closely related species of insects: Aedes aegypti and Culex quinquefasciatus. Here, we have experimentally confirmed the presence of these genes in mosquitoes and attempted to unveil their evolutionary history. A detailed study was conducted, including evaluation of taxonomic distribution, phylogenetic inferences and microsynteny analyses, indicating that mosquito RIP genes derived from a single Horizontal Gene Transfer (HGT) event, probably from a cyanobacterial donor species. Moreover, evolutionary analyses show that, after the HGT event, these genes evolved under purifying selection, strongly suggesting they play functional roles in these organisms. Ribosome inactivating proteins (RIPs, EC 3.2.2.22) irreversibly modify ribosomes through the depurination of an adenine residue in the conserved alpha-sarcin/ricin loop of 28S rRNA1–4. This modification prevents the binding of elongation factor 2 to the ribosome, arresting protein synthesis5, 6. The occurrence of RIP genes has been exper- imentally confirmed in a wide range of plant taxa, as well as in several species of Gram positive and Gram negative bacteria7–9. -
The Importance of Heritability in Psychological Research: the Case of Attitudes
Psychological Review Copyright 1993 by the American Psychological Association, Inc. 1993, Vol. 100, No. 1,129-142 0033-295X/93/S3.00 The Importance of Heritability in Psychological Research: The Case of Attitudes Abraham Tesser It is argued that differences in response heritability may have important implications for the testing of general psychological theories, that is, responses that differ in heritability may function differ- ently. For example, attitudes higher in heritability are shown to be responded to more quickly, to be more resistant to change, and to be more consequential in the attitude similarity attraction relation- ship. The substantive results are interpreted in terms of attitude strength and niche building. More generally, the implications of heritability for the generality and typicality of treatment effects are also discussed. Although psychologists clearly recognize the impact of genet- heritabilities is both long and surprising. As noted earlier, the ics on behavior, their theories rarely reflect this knowledge. intellectual abilities domain has received the most press, and Most theories assume that behavior is relatively plastic and is the genetic contribution to that domain is well documented shaped almost entirely by situational parameters. The possibil- (e.g., Loehlin, Willerman, & Horn, 1988; Plomin & Rende, ity that a response may have a high heritability is often ignored. 1991). There is also evidence of genetic contributions to spe- I argue here that ignoring this possibility is consequential. The cific cognitive abilities, school achievement, creativity, reading vehicle used in this article is attitudes. This vehicle was chosen disability, and mental retardation (see Plomin, 1989, for a re- because it is a domain with which I have some familiarity; it is a view). -
Mirror Neurons and Colamus Humanitatem Avances En Psicología Latinoamericana, Vol
Avances en Psicología Latinoamericana ISSN: 1794-4724 [email protected] Universidad del Rosario Colombia Skoyles, John R. Why our brains cherish humanity: Mirror neurons and colamus humanitatem Avances en Psicología Latinoamericana, vol. 26, núm. 1, junio, 2008, pp. 99-111 Universidad del Rosario Bogotá, Colombia Available in: http://www.redalyc.org/articulo.oa?id=79926108 How to cite Complete issue Scientific Information System More information about this article Network of Scientific Journals from Latin America, the Caribbean, Spain and Portugal Journal's homepage in redalyc.org Non-profit academic project, developed under the open access initiative Why our brains cherish humanity: Mirror neurons and colamus humanitatem JOHN R. SKOYLES* Centre for Mathematics and Physics in the Life Sciences and Experimental Biology (CoMPLEX) University College London, London, UK Centre for Philosophy of Natural and Social Science (CNPSS) London School of Economics, London, UK Abstract Resumen Commonsense says we are isolated. After all, our El sentido común dice que estamos aislados. Des- bodies are physically separate. But Seneca’s cola- pués de todo, nuestros cuerpos están separados mus humanitatem, and John Donne’s observation físicamente. Pero la obra Colamus humanitatem that “no man is an island” suggests we are neither de Séneca y la observación de que “ningún hombre entirely isolated nor separate. A recent discovery in es una isla”, que hizo John Donne, sugieren que no neuroscience—that of mirror neurons—argues that estamos ni completamente aislados ni separados. the brain and the mind is neither built nor functions Un descubrimiento reciente de la neurociencia, el remote from what happens in other individuals. -
Is the Germline Immortal and Continuous? a Discussion in Light of Ipscs and Germline Regeneration
Is the Germline Immortal and Continuous? A Discussion in Light of iPSCs and Germline Regeneration 1 1 Kate MacCord and B. Duygu Özpolat 1 - Marine Biological Laboratory, Woods Hole, MA, USA 1 ABSTRACT The germline gives rise to gametes, is the hereditary cell lineage, and is often called immortal and continuous. However, what exactly is immortal and continuous about the germline has recently come under scrutiny. The notion of an immortal and continuous germline has been around for over 130 years, and has led to the concept of a barrier between the germline and soma (the “Weismann barrier”). One repercussion of such a barrier is the understanding that when the germline is lost, soma cannot replace it, rendering the organism infertile. Recent research on induced pluripotent stem cells (iPSCs) and germline regeneration raise questions about the impermeability of the Weismann barrier and the designation of the germline as immortal and continuous. How we conceive of the germline and its immortality shapes what we perceive to be possible in animal biology, such as whether somatic cells contribute to the germline in some metazoans during normal development or regeneration. We argue that reassessing the universality of germline immortality and continuity across all metazoans leads to big and exciting open questions about the germ-soma cell distinction, cell reprogramming, germline editing, and even evolution. 2 1.0 Introduction The germline is the lineage of reproductive cells that includes gametes and their precursors, including primordial germ cells and germline stem cells. Because the germline gives rise to the gametes, it is the hereditary cell lineage, and is ultimately responsible for all cells in an organism’s body, including the next generation of the germline, stem cells, and other somatic cells.