scholarly journals When three traits make a line: Evolution of phenotypic plasticity and genetic assimilation through linear reaction norms in stochastic environments

2015 ◽  
Author(s):  
Torbjorn Ergon ◽  
Rolf Ergon
Keyword(s):  
Phenotypic Plasticity ◽  
Genetic Correlations ◽  
Reaction Norm ◽  
Genetic Effects ◽  
Environmental Perception ◽  
Genetic Assimilation ◽  
Reaction Norms ◽  
Environmental Value ◽  
Linear Reaction ◽  
Definition Of

Genetic assimilation results from selection on phenotypic plasticity, but quantitative genetics models of linear reaction norms considering intercept and slope as traits do not fully incorporate the process of genetic assimilation. We argue that intercept-slope reaction norm models are insufficient representations of genetic effects on linear reaction norms, and that considering reaction norm intercept as a trait is unfortunate because the definition of this trait relates to a specific environmental value (zero) and confounds genetic effects on reaction norm elevation with genetic effects on environmental perception. Instead we suggest a model with three traits representing genetic effects that respectively (i) are independent of the environment, (ii) alter the sensitivity of the phenotype to the environment, and (iii) determine how the organism perceives the environment. The model predicts that, given sufficient additive genetic variation in environmental perception, the environmental value at which reaction norms tend to cross will respond rapidly to selection after an abrupt environmental change, and eventually become equal to the new mean environment. This readjustment of the zone of canalization becomes completed without changes in genetic correlations, genetic drift or imposing any fitness costs on maintaining plasticity. The asymptotic evolutionary outcome of this three-trait linear reaction norm generally entails a lower degree of phenotypic plasticity than the two-trait model, and maximum expected fitness does not occur at the mean trait values in the population.

scholarly journals Maintenance of genetic variation in phenotypic plasticity: the role of environmental variation

2000 ◽  
Vol 76 (3) ◽  
pp. 295-304 ◽  
Author(s):  
GERDIEN de JONG ◽  
SERGEY GAVRILETS
Keyword(s):  
Genetic Variation ◽  
Phenotypic Plasticity ◽  
Temporal Variation ◽  
Genetic Variance ◽  
Reaction Norm ◽  
Reaction Norms ◽  
Stabilizing Selection ◽  
Variable Environment ◽  
Linear Reaction

We study genetic variation in phenotypic plasticity maintained by a balance between mutation and weak stabilizing selection. We consider linear reaction norms allowing for spatial and/or temporal variation in the environments of development and selection. We show that the overall genetic variation maintained does not depend on whether the trait is plastic or not. The genetic variances in height and slope of a linear reaction norm, and their covariance, are predicted to decrease with the variation in the environment. Non-pleiotropic loci influencing either height or slope are expected to decrease the genetic variance in slope relative to that in height. Decrease in the ratio of genetic variance in slope to genetic variance in height with increasing variation in the environment presents a test for the presence of loci that only influence the slope, and not the height. We use data on Drosophila to test the theory. In seven of eight pair-wise comparisons genetic variation in reaction norm is higher in a less variable environment than in a more variable environment, which is in accord with the model's predictions.

PSVII-27 Genetic analysis of disease resilience of nursery-to-finish pigs under a natural disease challenge model using reaction norms

2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 235-235
Author(s):  
Jian Cheng ◽  
KyuSang Lim ◽  
Austin Putz ◽  
Anna Wolc ◽  
John Harding ◽  
...  
Keyword(s):  
Genetic Model ◽  
Average Daily Gain ◽  
Genetic Correlations ◽  
Reaction Norm ◽  
Cubic Spline ◽  
Clinical Disease ◽  
Random Regression ◽  
Disease Phenotypes ◽  
Linear Reaction ◽  
Better Than

Abstract Disease resilience is the ability of an animal to maintain performance across environments with different disease challenge loads (CL) and can be quantified using random regression reaction norm models that describe phenotype as a function of CL. Objectives of this study were to: 1) develop measures of CL using growth rate and clinical disease phenotypes under a natural disease challenge; 2) evaluate genetic variation in disease resilience. Data used were late nursery and finisher growth rates and clinical disease phenotypes, including medical treatment and mortality rates, and subjective health scores, collected on 50 batches of 60/75 crossbred (LRxY) barrows under a polymicrobial natural disease challenge. All pigs were genotyped using a 650K SNP panel. Different CL were derived from estimates of contemporary group effects and used as environmental covariates in reaction norm analyses of average daily gain (ADG) and treatment rate (TRT). The CL were compared based on model loglikelihoods and estimates of genetic variance, using both linear and cubic spline reaction norm models. Linear reaction norm models fitted the data significantly better than the standard genetic model and the cubic spline models fitted the data significantly better than the linear reaction norm model for most traits. CL based on early finisher ADG provided the best fit for nursery ADG, while CL based on clinical disease phenotypes was best for finisher ADG and TRT. With increasing CL, estimates of heritability for ADG initially decreased and then increased, while estimates of heritability for TRT generally increased with CL. Genetic correlations were low between ADG or TRT at high versus low CL but high for close CLs. Results can be used to select more resilient pigs across different CL levels, or high-performance animals at a given CL level, or a combination of these. Funded by Genome Canada, Genome Alberta, USDA-NIFA, and PigGenCanada.

scholarly journals Selection on reaction norms, genetic correlations and constraints

1994 ◽  
Vol 64 (2) ◽  
pp. 115-125 ◽  
Author(s):  
Peter H. Van Tienderen ◽  
Hans P. Koelewijn
Keyword(s):  
Phenotypic Plasticity ◽  
Response Function ◽  
Genetic Correlations ◽  
Reaction Norm ◽  
The Other ◽  
Character State ◽  
Heterogeneous Environments ◽  
Local Selection ◽  
Biological Interpretation ◽  
The Relationship

SummaryTwo approaches to the evolution of phenotypic plasticity in heterogeneous environments have recently been put forward. The first focuses on selection on the character expression within each environment; plasticity is seen as a by-product of local selection in various habitats. The second approach focuses on selection on the parameters of the response function of genotypes, and selection is thought to change the frequencies of ‘plasticity’ genes that affect the function. This paper discusses the relationship between the two approaches, with emphasis on applications. A method is described that allows switching from one approach to the other. It is argued that character state and reaction norm approaches, while to a large extent interchangeable, usually differ in the response function chosen. This choice, however, may strongly affect the biological interpretation. The methods outlined in this paper permit one to look at the data from different perspectives in order to avoid this danger.

scholarly journals Neuroendocrine control of life histories: what do we need to know to understand the evolution of phenotypic plasticity?

2007 ◽  
Vol 363 (1497) ◽  
pp. 1589-1598 ◽  
Author(s):  
C(Kate). M Lessells
Keyword(s):  
Control System ◽  
Phenotypic Plasticity ◽  
Life Histories ◽  
Reaction Norm ◽  
Neuroendocrine System ◽  
Reaction Norms ◽  
Selection Pressures ◽  
Neuroendocrine Control ◽  
Optimal Reaction Norm ◽  
Optimal Reaction

Almost all life histories are phenotypically plastic: that is, life-history traits such as timing of breeding, family size or the investment in individual offspring vary with some aspect of the environment, such as temperature or food availability. One approach to understanding this phenotypic plasticity from an evolutionary point of view is to extend the optimality approach to the range of environments experienced by the organism. This approach attempts to understand the value of particular traits in terms of the selection pressures that act on them either directly or owing to trade-offs due to resource allocation and other factors such as predation risk. Because these selection pressures will between environments, the predicted optimal phenotype will too. The relationship expressing the optimal phenotype for different environments is the optimal reaction norm and describes the optimal phenotypic plasticity. However, this view of phenotypic plasticity ignores the fact that the reaction norm must be underlain by some sort of control system: cues about the environment must be collected by sense organs, integrated into a decision about the appropriate life history, and a message sent to the relevant organs to implement that decision. In multicellular animals, this control mechanism is the neuroendocrine system. The central question that this paper addresses is whether the control system affects the reaction norm that evolves. This might happen in two different ways: first, the control system will create constraints on the evolution of reaction norms if it cannot be configured to produce the optimal reaction norm and second, the control system will create additional selection pressures on reaction norms if the neuroendocrine system is costly. If either of these happens, a full understanding of the way in which selection shapes reaction norms must include details of the neuroendocrine control system. This paper presents the conceptual framework needed to explain what is meant by a constraint or cost being created by the neuroendocrine system and discusses the extent to which this occurs and some possible examples. The purpose of doing this is to encourage endocrinologists to take a fresh look at neuroendocrine mechanisms and help identify the properties of the system and situations in which these generate constraints and costs that impinge on the evolution of phenotypic plasticity.

scholarly journals Untangling the Components of Phenotypic Plasticity in Nonlinear Reaction Norms of Drosophila Mediopunctata Pigmentation

2016 ◽  
Author(s):  
Felipe Bastos Rocha ◽  
Louis Bernard Klaczko
Keyword(s):  
Phenotypic Plasticity ◽  
Genetic Architecture ◽  
Empirical Studies ◽  
Strong Association ◽  
Experimental Studies ◽  
Reaction Norm ◽  
Developmental Model ◽  
Reaction Norms ◽  
Mean Values ◽  
Local Plasticity

AbstractPhenotypic plasticity may evolve as a generalist strategy to cope with environmental heterogeneity. Empirical studies, however, rarely find results confirming this prediction. This may be related to constraints imposed by the genetic architecture underlying plasticity variation. Three components of plasticity are central to characterize its variation: the intensity of response, the direction of response and the total amount of change. Reaction norm functions are a key analytical tool in plasticity studies. The more complex they are, the more plasticity components will vary independently, requiring more parameters to be described. Experimental studies are continuously collecting results showing that actual reaction norms are often nonlinear. This demands an analytical framework – yet to be developed – capable of straightforwardly untangling plasticity components. In Drosophila mediopunctata, the number of dark spots on the abdomen decreases as a response to increasing developmental temperatures. We have previously described a strong association between reaction norm curvature and across-environment mean values in homozygous strains. Here, we describe seven new reaction norms of heterozygous genotypes and further the investigation on the genetic architecture of this trait’s plasticity, testing three competing models from the literature – Overdominance, Epistasis and Pleiotropy. We use the curves of localized slopes of each reaction norm – Local Plasticity functions – to characterize the plastic response intensity and direction, and introduce a Global Plasticity parameter to quantify their total amount of change. Uncoupling plasticity components allowed us to discard the Overdominance model, weaken the Epistasis model and strengthen the support for the Pleiotropy model. Furthermore, this approach allows the elaboration of a coherent developmental model for the pigmentation of D. mediopunctata where genetic variation at one single feature explains the patterns of plasticity and overall expression of the trait. We claim that Global Plasticity and Local Plasticity may prove instrumental to the understanding of adaptive reaction norm evolution

Phenotypic Plasticity

2001 ◽  
Author(s):  
Massimo Pigliucci
Keyword(s):  
Phenotypic Plasticity ◽  
Environmental Conditions ◽  
Environmental Changes ◽  
Reaction Norm ◽  
Reaction Norms ◽  
Genetic Constitution ◽  
Genotype 3 ◽  
Norm Of Reaction ◽  
Living Organisms ◽  
And Behavior

Phenotypic plasticity is the property of a genotype to produce different phenotypes in response to different environmental conditions (Bradshaw 1965; Mazer and Damuth, this volume, chapter 2). Simply put, students of phenotypic plasticity deal with the way nature (genes) and nurture (environment) interact to yield the anatomy, morphology, and behavior of living organisms. Of course, not all genotypes respond differentially to changes in the environment, and not all environmental changes elicit a different phenotype given a particular genotype. Furthermore, while the distinction between genotype and phenotype is in principle very clear, several complicating factors immediately ensue. For example, the genotype can be modified by environmental action, as in the case of DNA methylation patterns (e.g., Sano et al. 1990; Mazer and Damuth, this volume, chapter 2). More intuitively, since environments are constantly changed by the organisms that live in them, the genetic constitution of a population influences the environment itself. Perhaps the most intuitive way to visualize phenotypic plasticity is through what is termed a norm of reaction. This genotype-specific function relates the phenotypes produced to the environments in which they are produced. The figure presents a simple example with a population made of three different genotypes experiencing a series of environmental conditions. Genotype 1 yields a low phenotypic value toward the left end of the environmental continuum (say, an insect with small wings at low temperature) but a high phenotypic value at the opposite environmental extreme (say, large wings at high temperature). Genotype 3, however, does the exact opposite, while genotype 2 is unresponsive to environmental changes, always producing the same phenotype regardless of the conditions (within the range of environments considered). Even though the case presented in figure 5.1 is very simple (notice, for example, that the reaction norms are linear, which is unlikely in real situations), several general principles are readily understood following a closer analysis: . . . 1. Let us consider the relationship between phenotypic plasticity and reaction norms. While the two terms are often used as synonyms, they are clearly not. A reaction norm is the trajectory in environment- phenotype space that is typical of a given genotype; plasticity is the degree to which that reaction norm deviates from a flat line parallel to the environmental axis. . . .

Evolution of Reaction Norms

2020 ◽  
Author(s):  
Rebekah A. Oomen ◽  
Jeffrey A. Hutchings
Keyword(s):  
Phenotypic Plasticity ◽  
Environmental Variability ◽  
Nonlinear Function ◽  
Environmental Variation ◽  
Reaction Norm ◽  
Reaction Norms ◽  
Phenotypic Trait ◽  
Phenotypic Variance ◽  
Linear Quadratic ◽  
Norm Evolution

Phenotypic variance is a function of genetic variability, environmental variation, and the ways in which genetic and environmental variation interact, i.e., VG×E. Reaction norms are a means of conceptually, graphically, and mathematically describing this total variance and are a powerful tool for decomposing it into its constituent parts (i.e., nature, nurture, and, critically, their interaction). A reaction norm is defined as the range of phenotypes expressed by a genotype along an environmental gradient. It is represented by a linear or nonlinear function which describes the value of a phenotypic trait for a particular genotype or group of genotypes in different environments. As such, it is closely related to the concept of phenotypic plasticity, which can be represented by a reaction norm with a non-zero slope (i.e., the phenotype varies with respect to the environment). While the term (which originated as Reaktionsnorm) has been in use for over one hundred years, there has been some debate about the most appropriate way to describe it mathematically. Nonetheless, there is general consensus that a reaction norm has multiple properties, each of which can be the target of selection. Reaction norms are typically described as consisting of: (1) an intercept, elevation, or offset, which describes the mean trait value across all environments, (2) a slope, which quantifies the degree of trait plasticity, and (3) shape or curvature (e.g., linear, quadratic, monotonic). Evidence that trait means and plasticities can evolve separately underscores the necessity of applying a reaction norm framework for studying ecological and evolutionary responses to the environment, because measuring phenotypes in a single environmental context does not necessarily reflect their relative values or diversities in a different context. These contextual differences are particularly important in a world of rapid anthropogenic change and increasing environmental variability. Therefore, in addition to being fundamental to ecological and evolutionary phenomena, reaction norm evolution is relevant for diverse biological fields, including behavior and psychology, conservation and natural resource management, global change biology, agriculture and breeding programs, and human health. Given that evolutionary change is defined by genetic change, we focus this article on variation among reaction norms from different genotypes (i.e., reaction norms that have potentially evolved to be divergent from one another) as well as the forces that promote and constrain reaction norm evolution. For an overview of the literature on plasticity itself (keeping in mind that reaction norms need not be plastic), see the separate Oxford Bibliographies in Evolutionary Biology article Phenotypic Plasticity.

scholarly journals Thermal reaction norms in sperm performance of Atlantic cod (Gadus morhua)

2010 ◽  
Vol 67 (3) ◽  
pp. 498-510 ◽  
Author(s):  
Craig F. Purchase ◽  
Ian A.E. Butts ◽  
Alexandre Alonso-Fernández ◽  
Edward A. Trippel
Keyword(s):  
Phenotypic Plasticity ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Swimming Performance ◽  
Common Garden ◽  
Reaction Norm ◽  
Thermal Reaction ◽  
Reaction Norms ◽  
Experimental Unit ◽  
Environment Interaction

Phenotypic plasticity occurs when a genotype produces variable phenotypes under different environments; the shapes of such responses are known as norms of reaction. The genetic scale at which reaction norms can be determined is restricted by the experimental unit that can be exposed to variable environments. This has limited their description beyond the family level in higher organisms, thus hindering our understanding of differences in plasticity at the scale of the individual. Using a three-year common-garden experiment, we quantify reaction norms in sperm performance of individual genotypes within different families of Atlantic cod ( Gadus morhua ). Cod sperm showed phenotypic plasticity in swimming performance across temperatures (3, 6, 11, and 21 °C), but the pattern of the response depended upon how long sperm had been swimming (30, 60, 120, or 180 s), i.e., plasticity in plasticity. Sperm generally swam fastest at intermediate temperatures when first assessed at 30 s after activation. However, a significant genotype × environment interaction was present, indicating inter-individual differences in phenotypic plasticity. To our knowledge, this is the first study to describe variable sperm performance across environmental conditions as a reaction norm. The results have potential theoretical, conservation, and aquaculture implications.

scholarly journals Plasticity of lifespan: a reaction norm perspective

2014 ◽  
Vol 73 (4) ◽  
pp. 532-542 ◽  
Author(s):  
Thomas Flatt
Keyword(s):  
Phenotypic Plasticity ◽  
Reaction Norm ◽  
Reaction Norms ◽  
Specific Response ◽  
Plastic Response ◽  
General Phenomenon ◽  
Response Curves ◽  
Statistical Framework ◽  
Single Genotype ◽  
Molecular Aspects

It is a well-appreciated fact that in many organisms the process of ageing reacts highly plastically, so that lifespan increases or decreases when the environment changes. The perhaps best-known example of such lifespan plasticity is dietary restriction (DR), a phenomenon whereby reduced food intake without malnutrition extends lifespan (typically at the expense of reduced fecundity) and which has been documented in numerous species, from invertebrates to mammals. For the evolutionary biologist, DR and other cases of lifespan plasticity are examples of a more general phenomenon called phenotypic plasticity, the ability of a single genotype to produce different phenotypes (e.g. lifespan) in response to changes in the environment (e.g. changes in diet). To analyse phenotypic plasticity, evolutionary biologists (and epidemiologists) often use a conceptual and statistical framework based on reaction norms (genotype-specific response curves) and genotype × environment interactions (G × E; differences in the plastic response among genotypes), concepts that biologists who are working on molecular aspects of ageing are usually not familiar with. Here I briefly discuss what has been learned about lifespan plasticity or, more generally, about plasticity of somatic maintenance and survival ability. In particular, I argue that adopting the conceptual framework of reaction norms and G × E interactions, as used by evolutionary biologists, is crucially important for our understanding of the mechanisms underlying DR and other forms of lifespan or survival plasticity.

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