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Phenotypic Plasticity, Adaptive Plasticity

The Journal of Experimental Biology

Special issue on "Phenotypic Plasticity"

Volume 209, Issue 12, June 15, 2006

Edited by H. Hoppeler, M. Flück, K. Lukowiak, and T. Garland, Jr.

List of Papers and Abstracts

Martin Flück
Functional, structural and molecular plasticity of mammalian skeletal muscle in response to exercise stimuli
J Exp Biol 209: 2239-2248.

Ian A. Johnston
Environment and plasticity of myogenesis in teleost fish
J Exp Biol 209: 2249-2264.

David A. Hood, Isabella Irrcher, Vladimir Ljubicic, and Anna-Maria Joseph
Coordination of metabolic plasticity in skeletal muscle
J Exp Biol 209: 2265-2275.

Judy E. Anderson
The satellite cell as a companion in skeletal muscle plasticity: currency, conveyance, clue, connector and colander
J Exp Biol 209: 2276-2292.

P. V. Nguyen
Comparative plasticity of brain synapses in inbred mouse strains
J Exp Biol 209: 2293-2303.

Pierre J. Magistretti
Neuron–glia metabolic coupling and plasticity
J Exp Biol 209: 2304-2311.

Michael A. Colicos, and Naweed I. Syed
Neuronal networks and synaptic plasticity: understanding complex system dynamics by interfacing neurons with silicon technologies
J Exp Biol 209: 2312-2319.

Bernard Swynghedauw
Phenotypic plasticity of adult myocardium: molecular mechanisms
J Exp Biol 209: 2320-2327.

Andrew Cossins, Jane Fraser, Margaret Hughes, and Andrew Gracey
Post-genomic approaches to understanding the mechanisms of environmentally induced phenotypic plasticity
J Exp Biol 209: 2328-2336.

Chris Goldring, Neil Kitteringham, Rosalind Jenkins, Ian Copple, Jean-Francois Jeannin, and B. Kevin Park
Plasticity in cell defence: access to and reactivity of critical protein residues and DNA response elements
J Exp Biol 209: 2337-2343.

Theodore Garland, Jr, and Scott A. Kelly
Phenotypic plasticity and experimental evolution
J Exp Biol 209: 2344-2361. [PDF file]

Massimo Pigliucci, Courtney J. Murren, and Carl D. Schlichting
Phenotypic plasticity and evolution by genetic assimilation
J Exp Biol 209: 2362-2367.

Trevor D. Price
Phenotypic plasticity, sexual selection and the evolution of colour patterns
J Exp Biol 209: 2368-2376.

James A. Fordyce
The evolutionary consequences of ecological interactions mediated through phenotypic plasticity
J Exp Biol 209: 2377-2383.

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Summary 1 of 14
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Functional, structural and molecular plasticity of mammalian skeletal muscle in response to exercise stimuli

Martin Flück

Unit for Functional Anatomy, Department of Anatomy, University of Berne, Baltzerstrasse 2, Switzerland

e-mail: flueck@ana.unibe.ch

Accepted 6 February 2006

Summary

Biological systems have acquired effective adaptive strategies to cope with physiological challenges and to maximize biochemical processes under imposed constraints. Striated muscle tissue demonstrates a remarkable malleability and can adjust its metabolic and contractile makeup in response to alterations in functional demands. Activity-dependent muscle plasticity therefore represents a unique model to investigate the regulatory machinery underlying phenotypic adaptations in a fully differentiated tissue.

Adjustments in form and function of mammalian muscle have so far been characterized at a descriptive level, and several major themes have evolved. These imply that mechanical, metabolic and neuronal perturbations in recruited muscle groups relay to the specific processes being activated by the complex physiological stimulus of exercise. The important relationship between the phenotypic stimuli and consequent muscular modifications is reflected by coordinated differences at the transcript level that match structural and functional adjustments in the new training steady state. Permanent alterations of gene expression thus represent a major strategy for the integration of phenotypic stimuli into remodeling of muscle makeup.

A unifying theory on the molecular mechanism that connects the single exercise stimulus to the multi-faceted adjustments made after the repeated impact of the muscular stress remains elusive. Recently, master switches have been recognized that sense and transduce the individual physical and chemical perturbations induced by physiological challenges via signaling cascades to downstream gene expression events. Molecular observations on signaling systems also extend the long-known evidence for desensitization of the muscle response to endurance exercise after the repeated impact of the stimulus that occurs with training. Integrative approaches involving the manipulation of single factors and the systematic monitoring of downstream effects at multiple levels would appear to be the ultimate method for pinpointing the mechanism of muscle remodeling. The identification of the basic relationships underlying the malleability of muscle tissue is likely to be of relevance for our understanding of compensatory processes in other tissues, species and organisms.

Key words: exercise, endurance, hypoxia, gene, transcriptome, morphometry, microarray, PCR

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Summary 2 of 14
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Environment and plasticity of myogenesis in teleost fish

Ian A. Johnston

Gatty Marine Laboratory, School of Biology, University of St Andrews, St Andrews, Fife, KY16 8LB, Scotland, UK

e-mail: iaj@st-andrews.ac.uk

Accepted 7 February 2006

Summary

Embryonic development in teleosts is profoundly affected by environmental conditions, particularly temperature and dissolved oxygen concentrations. The environment determines the rate of myogenesis, the composition of sub-cellular organelles, patterns of gene expression, and the number and size distribution of muscle fibres. During the embryonic and larval stages, muscle plasticity to the environment is usually irreversible due to the rapid pace of ontogenetic change. In the early life stages, muscle can affect locomotory performance and behaviour, with potential consequences for larval survival. Postembryonic growth involves myogenic progenitor cells (MPCs) that originate in the embryo. The embryonic temperature regime can have long-term consequences for the growth of skeletal muscle in some species, including the duration and intensity of myotube formation in adult stages. In juvenile and adult fish, abiotic (temperature, day-length, water flow characteristics, hypoxia) and biotic factors (food availability, parasitic infection) have complex effects on the signalling pathways regulating the proliferation and differentiation of MPCs, protein synthesis and degradation, and patterns of gene expression. The phenotypic responses observed to the environment frequently vary during ontogeny and are integrated with endogenous physiological rhythms, particularly sexual maturation. Studies with model teleosts provide opportunities for investigating the underlying genetic mechanisms of muscle plasticity that can subsequently be applied to non-model species of more ecological or commercial interest.

Key words: temperature, oxygen, myotomal muscle, environmental genomics, phenotypic plasticity, ectotherm, developmental plasticity, skeletal muscle

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Summary 3 of 14
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Coordination of metabolic plasticity in skeletal muscle

David A. Hood1,2,*, Isabella Irrcher2, Vladimir Ljubicic1 and Anna-Maria Joseph2

1 School of Kinesiology and Health Science, York University, Toronto, Ontario, M3J 1P3, Canada
2 Department of Biology, York University, Toronto, Ontario, M3J 1P3, Canada

* Author for correspondence (e-mail: dhood@yorku.ca)

Accepted 21 February 2006

Summary

Skeletal muscle is a highly malleable tissue, capable of pronounced metabolic and morphological adaptations in response to contractile activity (i.e. exercise). Each bout of contractile activity results in a coordinated alteration in the expression of a variety of nuclear DNA and mitochondrial DNA (mtDNA) gene products, leading to phenotypic adaptations. This results in an increase in muscle mitochondrial volume and changes in organelle composition, referred to as mitochondrial biogenesis. The functional consequence of this biogenesis is an improved resistance to fatigue. Signals initiated by the exercise bout involve changes in intracellular Ca2+ as well as alterations in energy status (i.e. ATP/ADP ratio) and the consequent activation of downstream kinases such as AMP kinase and Ca2+-calmodulin-activated kinases. These kinases activate transcription factors that bind DNA to affect the transcription of genes, the most evident manifestation of which occurs during the post-exercise recovery period when energy metabolism is directed toward anabolism, rather than contractile activity. An important protein that is affected by exercise is the transcriptional coactivator PGC-1, which cooperates with multiple transcription factors to induce the expression of nuclear genes encoding mitochondrial proteins. Once translated in the cytosol, these mitochondrially destined proteins are imported into the mitochondrial outer membrane, inner membrane or matrix space via specific import machinery transport components. Contractile activity affects the expression of the import machinery, as well as the kinetics of import, thus facilitating the entry of newly synthesized proteins into the expanding organelle. An important set of proteins that are imported are the mtDNA transcription factors, which influence the expression and replication of mtDNA. While mtDNA contributes only 13 proteins to the synthesis of the organelle, these proteins are vital for the proper assembly of multi-subunit complexes of the respiratory chain, when combined with nuclear-encoded protein subunits. The expansion of skeletal muscle mitochondria during organelle biogenesis involves the assembly of an interconnected network system (i.e. a mitochondrial reticulum). This expansion of membrane size is influenced by the balance between mitochondrial fusion and fission. Thus, mitochondrial biogenesis is an adaptive process that requires the coordination of multiple cellular events, including the transcription of two genomes, the synthesis of lipids and proteins and the stoichiometric assembly of multisubunit protein complexes into a functional respiratory chain. Impairments at any step can lead to defective electron transport, a subsequent failure of ATP production and an inability to maintain energy homeostasis.

Key words: mitochondrial biogenesis, transcription factors, reactive oxygen species, calcium signaling, mitochondrial protein import

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Summary 4 of 14
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The satellite cell as a companion in skeletal muscle plasticity: currency, conveyance, clue, connector and colander

Judy E. Anderson

Department of Human Anatomy and Cell Science, Faculty of Medicine, University of Manitoba, Winnipeg, MB, R3E 0W3, Canada

Author for correspondence (e-mail: janders@ms.umanitoba.ca)

Accepted 11 January 2006

Summary

Satellite cells are companions to voluntary muscle fibres, and are named for their intimate positional or `satellite' relationship, as if revolving around fibres, like a satellite moon around the earth. Studies on the nature of at least some satellite cells, including their capabilities for self-renewal and for giving rise to multiple lineages in a stem cell-like function, are exploring the molecular basis of phenotypes described by markers of specialized function and gene expression in normal development, neuromuscular disease and aging. In adult skeletal muscle, the self-renewing capacity of satellite cells contributes to muscle growth, adaptation and regeneration. Muscle remodeling, such as demonstrated by changes in myofibre cross-sectional area and length, nerve and tendon junctions, and fibre-type distribution, occur in the absence of injury and provide broad functional and structural diversity among skeletal muscles. Those contributions to plasticity involve the satellite cell in at least five distinct roles, here described using metaphors for behaviour or the investigator's perspective. Satellite cells are the `currency' of muscle; have a `conveyance' role in adaptation by domains of cytoplasm along a myofibre; serve researchers, through a marker role, as `clues' to various activities of muscle; are `connectors' that physically, and through signalling and cell-fibre communications, bridge myofibres to the intra- and extra-muscular environment; and are equipped as metabolic and genetic filters or `colanders' that can rectify or modulate particular signals. While all these roles are still under exploration, each contributes to the plasticity of skeletal muscle and thence to the overall biology and function of an organism. The use of metaphor for describing these roles helps to clarify and scrutinize the definitions that form the basis of our understanding of satellite cell biology: the metaphors provide the construct for various approaches to detect or test the nature of satellite cell functions in skeletal muscle plasticity.

Key words: muscle regeneration, activation, myogenesis, fibre, nitric oxide, gene expression, heterogeneity, transplantation

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Summary 5 of 14
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Comparative plasticity of brain synapses in inbred mouse strains

P. V. Nguyen

Laboratory of Synaptic Plasticity, Department of Physiology and Centre for Neuroscience, University of Alberta School of Medicine, Medical Sciences Building, Edmonton, T6G 2H7, Canada

e-mail: Peter.Nguyen@ualberta.ca

Accepted 14 November 2005

Summary

One niche of experimental biology that has experienced considerable progress is the neurobiology of learning and memory. A key contributor to such progress has been the widespread use of transgenic and `knockout' mice to elucidate the mechanisms of identifiable phenotypes of learning and memory. Inbred mouse strains are needed to generate genetically modified mice. However, genetic variations between inbred strains can confound the interpretation of cellular neurophysiological phenotypes of mutant mice. It is known that altered physiological strength of synaptic transmission (`synaptic plasticity') can modify and regulate learning and memory. Characterization of the synaptic phenotypes of inbred mouse strains is needed to identify the most appropriate strains to use for generating mutant mouse models of memory function. More importantly, comparative electrophysiological analyses of inbred mice per se can also shed light on which forms of synaptic plasticity underlie particular types of learning and memory. Many such analyses have focused on synaptic plasticity in the hippocampus because of the critical roles of this brain structure in the formation and consolidation of long-term memories. Comparative electrophysiological data obtained from several inbred mouse strains are reviewed here to highlight the following key notions: (1) synaptic plasticity is influenced by the genetic backgrounds of inbred mice; (2) the plasticity of hippocampal synapses in inbred mice is `tuned' to particular temporal patterns of activity; (3) long-term potentiation, but not long-term depression, is a cellular correlate of behavioural memory performance in some strains; (4) synaptic phenotyping of inbred mouse strains can identify cellular models of memory impairment that can be used to elucidate mechanisms that may cause specific memory deficits.

Key words: synaptic plasticity, hippocampus, inbred mice, mouse strain, long-term potentiation (LTP), long-term depression (LTD), learning, memory

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Summary 6 of 14
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Neuron–glia metabolic coupling and plasticity

Pierre J. Magistretti

Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), Switzerland and Centre de Neurosciences Psychiatriques, CHUV, Departement de Psychiatrie, Site de Cery, CH1008 Prilly/Lausanne, Switzerland

e-mail: pierre.magistretti@unil.ch

Accepted 14 March 2006

Summary

The coupling between synaptic activity and glucose utilization (neurometabolic coupling) is a central physiological principle of brain function that has provided the basis for 2-deoxyglucose-based functional imaging with positron emission tomography (PET). Astrocytes play a central role in neurometabolic coupling, and the basic mechanism involves glutamate-stimulated aerobic glycolysis; the sodium-coupled reuptake of glutamate by astrocytes and the ensuing activation of the Na-K-ATPase triggers glucose uptake and processing via glycolysis, resulting in the release of lactate from astrocytes. Lactate can then contribute to the activity-dependent fuelling of the neuronal energy demands associated with synaptic transmission. An operational model, the `astrocyte–neuron lactate shuttle', is supported experimentally by a large body of evidence, which provides a molecular and cellular basis for interpreting data obtained from functional brain imaging studies. In addition, this neuron–glia metabolic coupling undergoes plastic adaptations in parallel with adaptive mechanisms that characterize synaptic plasticity. Thus, distinct subregions of the hippocampus are metabolically active at different time points during spatial learning tasks, suggesting that a type of metabolic plasticity, involving by definition neuron–glia coupling, occurs during learning. In addition, marked variations in the expression of genes involved in glial glycogen metabolism are observed during the sleep–wake cycle, with in particular a marked induction of expression of the gene encoding for protein targeting to glycogen (PTG) following sleep deprivation. These data suggest that glial metabolic plasticity is likely to be concomitant with synaptic plasticity.

Key words: neuro-metabolic coupling, plasticity, astrocyte, glia, sleep–wake cycle

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Summary 7 of 14
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Neuronal networks and synaptic plasticity: understanding complex system dynamics by interfacing neurons with silicon technologies

Michael A. Colicos1,* and Naweed I. Syed2

1 Department of Physiology and Biophysics, Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, T2N 4N1, Canada
2 Department of Cell Biology and Anatomy, Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, T2N 4N1, Canada

* Author for correspondence (e-mail: mcolicos@ucalgary.ca)

Accepted 8 February 2006

Summary

Information processing in the central nervous system is primarily mediated through synaptic connections between neurons. This connectivity in turn defines how large ensembles of neurons may coordinate network output to execute complex sensory and motor functions including learning and memory. The synaptic connectivity between any given pair of neurons is not hard-wired; rather it exhibits a high degree of plasticity, which in turn forms the basis for learning and memory. While there has been extensive research to define the cellular and molecular basis of synaptic plasticity, at the level of either pairs of neurons or smaller networks, analysis of larger neuronal ensembles has proved technically challenging. The ability to monitor the activities of larger neuronal networks simultaneously and non-invasively is a necessary prerequisite to understanding how neuronal networks function at the systems level. Here we describe recent breakthroughs in the area of various bionic hybrids whereby neuronal networks have been successfully interfaced with silicon devices to monitor the output of synaptically connected neurons. These technologies hold tremendous potential for future research not only in the area of synaptic plasticity but also for the development of strategies that will enable implantation of electronic devices in live animals during various memory tasks.

Key words: synapse, transistor, photoconductive stimulation, interface, neural circuits, biocomputational device, biomic hybrid

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Summary 8 of 14
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Phenotypic plasticity of adult myocardium: molecular mechanisms

Bernard Swynghedauw

Inserm U.572, Hôpital Lariboisière, 41 Bd de la Chapelle, 75475, Paris Cedex 10, France

e-mail: Bernard.Swynghedauw@larib.inserm.fr

Accepted 10 January 2006

Summary

Cardiac phenotypic plasticity (so-called cardiac remodelling, CR) is characterized by changes in myocardial structure that happen in response to either mechanical overload or a loss of substance such as that occurring after myocardial infarction.

Mechanosensation is a widespread biological process and is inextricably mixed with other transduction systems from hormones and vasopeptides, which ultimately produce post-translational modifications of transcription factors. The expression of the four main transcription factors during cardiogenesis is also enhanced as a link to foetal reprogramming.

CR results from re-expression of the foetal programme, which is mostly adaptive, but also from several other phenotypic modifications that are not usually adaptive, such as fibrosis. (i) The initial determinant is mechanical, and re-expression of the foetal programme includes a global increase in genetic expression with cardiac hypertrophy, re-expression of genes that are normally not expressed in the adult ventricles, repression of genes not expressed during the foetal life, and activation of pre-exisiting stem cells. Microarray technology has revealed a coordinated change in expression of genes pertaining to signal transduction, metabolic function, structure and motility, and cell organism defence. The physiological consequence is a better adapted muscle. (ii) During clinical conditions, the effects of mechanics are modified by several interfering determinants that modify CR, including senescence, obesity, diabetes, ischemia and the neurohormonal reaction. Each of these factors can alter myocardial gene expression and modify molecular remodelling of mechanical origin.

Finally, as compared to evolutionary phenotypic plasticity described in plants and insects in response to variations in environmental conditions, in CR, the environmental factor is internal, plasticity is primarily adaptive, and it involves coordinated changes in over 1400 genes. Study of reaction norms showed that the genotypes from different animal species are similarly plastic, but there are transgenic models in which adaptation to mechanics is not caused by hypertrophy but by qualitative changes in gene expression.

Key words: cardiac remodelling, phenotypic plasticity, foetal programme, myosin, energetics, heart failure, mechanoconversion

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Summary 9 of 14
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Post-genomic approaches to understanding the mechanisms of environmentally induced phenotypic plasticity

Andrew Cossins1,*, Jane Fraser1, Margaret Hughes1 and Andrew Gracey2

1 School of Biological Sciences, University of Liverpool, Crown Street, Liverpool L69 7ZB, UK
2 Marine Environmental Biology, University of Southern California, 3616 Trousdale Parkway, Los Angeles, CA 90089, USA

* Author for correspondence (e-mail: cossins@liv.ac.uk)

Accepted 5 April 2006

Summary

Post-genomic techniques offer new and detailed insights into the mechanisms underpinning all biological processes, including phenotypic plasticity and environmentally relevant phenotypes. Although they require access to genomic resources it is now possible to create these for species of comparative or environmental interest even within a modest research project. Here we describe an open transcript screen for genes responding to environmental cold that might account for the acquired cold-specific phenotype in all its complex manifestations. Construction of a cDNA microarray led to a survey of transcript expression levels in seven tissues of carp, as a function of time, and three different extents of cooling. The resulting data delineated a common stress response found in all tissues that comprises genes involved in cellular homeostasis, including energy charge, ATP turnover, protein turnover and stress protein production. These genes respond to kinds of perturbation other than cold and probably form part of a more general stress response common to other species. We also defined tissue-specific response patterns of transcript regulation whose main characteristics were investigated by a profiling technique based on categorisation of gene function. These genes underpin the highly tissue-specific pattern of physiological adaptations observed in the cold-acclimated fish. As a result we have identified a large number of candidate gene targets with which to investigate adaptive responses to environmental challenge.

Key words: transcriptomics, microarray, cDNA, carp, Cyprinus carpio

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Summary 10 of 14
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Plasticity in cell defence: access to and reactivity of critical protein residues and DNA response elements

Chris Goldring1,*, Neil Kitteringham1, Rosalind Jenkins1, Ian Copple1, Jean-Francois Jeannin2 and B. Kevin Park1

1 Department of Pharmacology and Therapeutics, University of Liverpool, Sherrington Buildings, Ashton Street, Liverpool L69 3GE, Merseyside, UK
2 Cancer Immunotherapy Laboratory, Ecole Pratique des Hautes Etudes, INSERM U517, Faculty of Medicine, Dijon, France

* Author for correspondence (e-mail: C.E.P.Goldring@liv.ac.uk)

Accepted 14 March 2006

Summary

Cellular and whole organ defence against pathogenic or chemical challenge is manifest as an adaptive response. Where appropriate, this may lead to induction of a cellular defence programme, thereby enhancing cell survival. When the challenge is overwhelming, the defence is breached and a switch is made to yield cell death, either by apoptosis or necrosis. Thus, a cell will defend itself where possible, but in extremis, it may recognise the futility of its resistance and allow itself to die. Transcription factor activation and access to the DNA regulatory elements that control a particular pattern of expression of defence genes is a major issue that may ultimately decide the fate of a cell in a changed environment. It is possible to visualise the access to the nucleus and to the genome, of paradigm gene loci or transcription factors, using a number of molecular techniques such as chromatin immunoprecipitation, in vivo footprinting and live/whole cell imaging. These methods are informative as to the array of transcription factors that may regulate a given gene, as well as the transitory nature of the transcriptional activation. The initial triggering of active transcription factor complexes typically occurs within the cytoplasm of the cell. Protein–protein interactions and signal transduction pathways, elucidated using a classical molecular genetics approach, have long been recognised as pivotal to the initial control of the levels and activity of transcription factors. We can now visualise modifications in critical residues of transcription factors and regulators during cellular response to chemical stress. These modifications may yield enhanced or repressed activity of transcription factors, they may be non-covalent or covalent, and they may occur in response to a variety of classes of chemicals. Such promiscuous signalling can provide plasticity in the cellular response to a wide array of chemical agents.

Key words: adaptation, proteins, stress, footprinting, transcription, iNOS, Nrf2, Keap1

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Summary 11 of 14
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Phenotypic plasticity and experimental evolution [PDF file]

Theodore Garland, Jr* and Scott A. Kelly

Department of Biology, University of California, Riverside, Riverside, CA 92521, USA

* Author for correspondence (e-mail: tgarland@ucr.edu)

Accepted 29 March 2006

Summary

Natural or artificial selection that favors higher values of a particular trait within a given population should engender an evolutionary response that increases the mean value of the trait. For this prediction to hold, the phenotypic variance of the trait must be caused in part by additive effects of alleles segregating in the population, and also the trait must not be too strongly genetically correlated with other traits that are under selection. Another prediction, rarely discussed in the literature, is that directional selection should favor alleles that increase phenotypic plasticity in the direction of selection, where phenotypic plasticity is defined as the ability of one genotype to produce more than one phenotype when exposed to different environments. This prediction has received relatively little empirical attention. Nonetheless, many laboratory experiments impose selection regimes that could allow for the evolution of enhanced plasticity (e.g. desiccation trials with Drosophila that last for several hours or days). We review one example that involved culturing of Drosophila on lemon for multiple generations and then tested for enhanced plasticity of detoxifying enzymes. We also review an example with vertebrates that involves selective breeding for high voluntary activity levels in house mice, targeting wheel-running behavior on days 5+6 of a 6-day wheel exposure. This selection regime allows for the possibility of wheel running itself or subordinate traits that support such running to increase in plasticity over days 1–4 of wheel access. Indeed, some traits, such as the concentration of the glucose transporter GLUT4 in gastrocnemius muscle, do show enhanced plasticity in the selected lines over a 5–6 day period. In several experiments we have housed mice from both the Selected (S) and Control (C) lines with or without wheel access for several weeks to test for differences in plasticity (training effects). A variety of patterns were observed, including no training effects in either S or C mice, similar changes in both the S and C lines, greater changes in the S lines but in the same direction in the C lines, and even opposite directions of change in the S and C lines. For some of the traits that show a greater training effect in the S lines, but in the same direction as in C lines, the greater effect can be explained statistically by the greater wheel running exhibited by S lines (`more pain, more gain'). For others, however, the differences seem to reflect inherently greater plasticity in the S lines (i.e. for a given amount of stimulus, such as wheel running/day, individuals in the S lines show a greater response as compared with individuals in the C lines). We suggest that any selection experiment in which the selective event is more than instantaneous should explore whether plasticity in the appropriate (adaptive) direction has increased as a component of the response to selection.

Key words: adaptive plasticity, artificial selection, complex traits, environment, exercise, genotype, locomotion, mouse

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Summary 12 of 14
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Phenotypic plasticity and evolution by genetic assimilation

Massimo Pigliucci1,*, Courtney J. Murren2 and Carl D. Schlichting3

1 Department of Ecology and Evolution, SUNY-Stony Brook, 650 Life Science Building, Stony Brook NY 11794, USA
2 Department of Biology, College of Charleston, Charleston, SC 29424, USA
3 Department of Ecology Evolutionary Biology, University of Connecticut, Storrs, CT 06269, USA

* Author for correspondence (e-mail: pigliucci@genotypbyenvironment.org)

Accepted 3 January 2006

Summary

In addition to considerable debate in the recent evolutionary literature about the limits of the Modern Synthesis of the 1930s and 1940s, there has also been theoretical and empirical interest in a variety of new and not so new concepts such as phenotypic plasticity, genetic assimilation and phenotypic accommodation. Here we consider examples of the arguments and counter-arguments that have shaped this discussion. We suggest that much of the controversy hinges on several misunderstandings, including unwarranted fears of a general attempt at overthrowing the Modern Synthesis paradigm, and some fundamental conceptual confusion about the proper roles of phenotypic plasticity and natural selection within evolutionary theory.

Key words: phenotypic plasticity, genetic assimilation, phenotypic accommodation, Modern Synthesis, natural selection, evolution

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Summary 13 of 14
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Phenotypic plasticity, sexual selection and the evolution of colour patterns

Trevor D. Price

Department of Ecology and Evolution, University of Chicago, Chicago, IL 60637, USA

e-mail: pricet@uchicago.edu

Accepted 21 February 2006

Summary

When a population comes to occupy a new environment, phenotypically plastic responses alter the distribution of phenotypes, and hence affect both the direction and the intensity of selection. Rates of evolution can be accelerated or retarded compared to what would happen in the absence of plasticity. Plastic responses in one trait result in novel selection pressures on other traits, and this can lead to evolution in completely different directions than predicted in the absence of plasticity. In this paper I use the concept of the adaptive surface in order to identify conditions under which the various different outcomes are expected. I then discuss differences between sexually and naturally selected traits. Sexually selected traits are often expected to be plastic in their expression, with individuals in high condition developing greater elaboration. As examples of sexually selected traits I review the evolution of colour patterns in birds with a view to assessing the magnitude of plastic responses in their development, and to ask how such responses may have influenced genetic evolution. The common colour pigments in birds are carotenoids and melanins. Both are used in social signaling, and consequently are expected to evolve to be phenotypically plastic indicators of an individual's quality. Perhaps partly because they are condition indicators, the quantity of carotenoids in the plumage can be strongly influenced by diet. Examples are described where alterations of carotenoids in the diet are thought to have altered the phenotype, driving genetic evolution in novel directions. Melanin patterns seem to be less affected by diet, but the intensity of melanization after moult is affected by social interactions during the moult and by raising birds in humid conditions. Hormonal manipulations can have dramatic effects on both the kinds of melanin produced (eumelanin or phaeomelanin) as well as the patterns they form. Differences between species in melanin patterns resemble differences produced by environmental manipulations, as well as those produced by simple modulations of parameters in computer simulations of pattern formation. While phenotypic plasticity is one way that genetic change in plumage patterns (and other traits) could be driven, there are others, including the appearance of major mutations and selection on standing variation whose distribution is not altered in the new environment. I consider some evidence for the different alternatives, and ask when they might lead to qualitatively different evolutionary outcomes.

Key words: carotenoid, colour pattern, melanin, plasticity, sexual selection

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Summary 14 of 14
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The evolutionary consequences of ecological interactions mediated through phenotypic plasticity

James A. Fordyce

Department of Ecology and Evolutionary Biology, University of Tennessee, Knoxville, TN 37996, USA

e-mail: jfordyce@utk.edu

Accepted 13 April 2006

Summary

Phenotypic plasticity describes the capacity of a genotype to exhibit a range of phenotypes in response to variation in the environment. Environmental variation encompasses both abiotic and biotic components of the environment, including interactions among organisms. The strength and outcome of many ecological interactions, ranging from antagonism to mutualism, are mediated through the phenotypically plastic responses of one or more players in the interaction. Herein, three broadly defined, non-mutually exclusive, evolutionary consequences of ecological interactions mediated through phenotypic plasticity are discussed. (1) The predictable plastic response of one partner can favor behaviors, physiological responses, and life history traits of an interacting partner that manipulate, circumvent, or ameliorate the response of that partner. (2) Phenotypic plasticity can generate substantial spatial and temporal variation within and among populations. Such phenotypic variation can depend on the density and identity of interacting players in an ecological community, and can ultimately affect the evolutionary outcome of ecological interactions. (3) Phenotypic plasticity affects the strength and direction of natural selection. Ecological interactions mediated through phenotypic plasticity are ubiquitous in nature, and the potential evolutionary consequences of these interactions illustrate the complexity inherent in understanding evolution in a community context.

Key words: adaptation, coevolution, ecological interaction, herbivory, induced response, natural selection, phenotypic plasticity, predation, variation