THE DETERMINATION OF GENETIC COVARIANCES AND PREDICTION OF EVOLUTIONARY TRAJECTORIES BASED ON A GENETIC CORRELATION MATRIX

There is much interest in measuring selection, quantifying evolutionary constraints, and predicting evolutionary trajectories in natural populations. For these studies, genetic (co)variances among fitness traits play a central role. We explore the conditions that determine the sign of genetic covariances and demonstrate a critical role of selection in shaping genetic covariances. In addition, we show that genetic covariance matrices rather than genetic correlation matrices should be characterized and studied in order to infer genetic basis of population differentiation and/or to predict evolutionary trajectories.     

GENETIC VARIATION AND THE EVOLUTION OF EPIGENETIC REGULATION

Epigenetic variation has been observed in a range of organisms, leading to questions of the adaptive significance of this variation. In this study, we present a model to explore the ecological and genetic conditions that select for epigenetic regulation. We find that the rate of temporal environmental change is a key factor controlling the features of this evolution. When the environment fluctuates rapidly between states with different phenotypic optima, epigenetic regulation may evolve but we expect to observe low transgenerational inheritance of epigenetic states, whereas when this fluctuation occurs over longer time scales, regulation may evolve to generate epigenetic states that are inherited faithfully for many generations. In all cases, the underlying genetic variation at the epigenetically regulated locus is a crucial factor determining the range of conditions that allow for evolution of epigenetic mechanisms.     

ORIGINS AND EVOLUTION OF A TRANSMISSIBLE CANCER

Canine transmissible venereal tumor (CTVT) is an infectious disease of dogs. Remarkably, the infectious agent is the cancerous cell itself. To investigate its origin and spread, we collected 37 tumor samples from four continents and determined their evolutionary relationships using microsatellite length differences and microarray-based comparative genomic hybridization (aCGH). The different tumors show very little microsatellite variation, and the pattern of variation that does exist is consistent with a purely asexual mode of transmission. Approximately one quarter of the loci scored by aCGH show copy number variation relative to normal dogs, again with little variation among different tumor samples. Sequence analysis of the RPPH1 gene indicates an origin from either dogs or wolves, and microsatellite analysis indicates that the tumor is more than 6000 years old, and perhaps originated when dogs were first domesticated. By contrast, the common ancestor of extant tumors lived within the last few hundred years, long after the first tumor. The genetic and genomic patterns we observe are typical of those expected of asexual pathogens, and the extended time since first origin may explain the many remarkable adaptations that have enabled this mammalian cell lineage to live as a unicellular pathogen.     

PHENOTYPIC PLASTICITY IN CHRYSOPERLA: GENETIC VARIATION IN THE SENSORY MECHANISM AND IN CORRELATED REPRODUCTIVE TRAITS

A genetically variable sensory mechanism provides phenotypic plasticity in the seasonal cycle of the Chrysoperla carnea species-complex of green lacewings. The mechanism functions as a switch during the pupal and early imaginal stages to determine aestival reproduction versus aestival dormancy, and it has two major components: (1) response to photoperiod and (2) response to a stimulus(i) associated with the prey of the larvae. Ultimately, the switch is based on the response to photoperiod—an all-or-nothing trait whose variation (long-day reproduction versus a short-day/long-day requirement for reproduction) is determined by alleles at two unlinked autosomal loci. In eastern North America, variation in this component of the switch differentiates two reproductively isolated “species” that are sympatric throughout the region: Chrysoperla carnea, in which both loci are homozygous for the dominant alleles that determine long-day, spring and summer reproduction and thus multivoltinism, and C. downesi, which has a very high incidence of the recessive alleles for the short-day/long-day requirement, and thus univoltine spring breeding. In contrast, geographical populations in western North America harbor variable amounts of within-and among-family genetic variation for the photoperiodic responses and also for the switch's second component—adult responsiveness to the prey of the larvae. The geographic pattern of genetic variation in the two components of the switch indicates that it is a highly integrated adaptation to environmental heterogeneity. Expression of among-family variation in the prey component of the switch is highly dependent on photoperiodic conditions and genotype (it requires a constant long daylength and the recessive short-day/long-day genotype). Thus, we infer that responsiveness to prey evolved as a modifier of the photoperiodic trait. The switch has a significant negative effect on a major determinant of fitness; it lengthens the preoviposition period in nondiapausing reproductives. This negative effect may result in temporal variation in the direction of selection, which helps maintain genetic variability in the switch mechanisms of western populations. Also, the photoperiodic and prey components of the switch are positively correlated with fecundity in nondiapausing reproductives; however, the strong influence of environmental factors—presence or absence of prey—leaves open the question whether the correlated effects on fecundity are expressed in nature.     

QUANTITATIVE GENETICS OF BRYOZOAN PHENOTYPIC EVOLUTION. III. PHENOTYPIC PLASTICITY AND THE MAINTENANCE OF GENETIC VARIATION

Cheilostome bryozoan species show long-term morphologic stasis, implying stabilizing selection sustained for millions of years, but nevertheless retain significant heritable variation in traits of skeletal morphology. The possible role of within-genotype (within-colony) phenotypic variability in preserving genetic diversity was analyzed using breeding data for two species of Stylopoma from sites along 110 km of the Caribbean coast of Panama. Variation among zooids within colonies accounts for nearly two-thirds of the phenotypic variance on average, increases with environmental heterogeneity, and includes significant genotype-environment interaction. Thus, within-colony variability apparently represents phenotypic plasticity, at least some of which is heritable, rather than random “developmental noise.” Almost all of the among-colonies component of phenotypic variance is accounted for by additive genetic differences in trait means, suggesting that within-colony plasticity includes virtually all of the environmental component of phenotypic variance in these populations of Stylopoma. Thus, heritable within-colony plasticity could play a significant part in maintaining genetic diversity in cheilostomes, but it is also possible that rates of polygenic mutation alone are sufficient to balance the effects of selection.     

A GENETIC PERSPECTIVE OF MAMMALIAN VARIATION AND EVOLUTION IN THE INDONESIAN ARCHIPELAGO: BIOGEOGRAPHIC CORRELATES IN THE FRUIT BAT GENUS CYNOPTERUS

This study investigated allozyme and morphometric variability within the genus Cynopterus, with particular emphasis on C. nusatenggara, which is endemic to Wallacea, the area encompassing the Oriental-Australian biogeographic interface. The genetic distances between Cynopterus species are small by mammalian standards and suggest that this genus has undergone a recent series of speciation events. The genetic distance between populations of C. nusatenggara is strongly correlated with both the contemporary sea-crossing distance between islands and the estimated sea crossing at the time of the last Pleistocene glacial maximum, 18,000 b .p . This observation, together with low levels of population substructure within islands as shown by F-statistics, indicates that the sea is a primary and formidable barrier to gene exchange. The genetic distance and the great-circle geographical distance between the populations of C. nusatenggara are not correlated, although a principal-coordinates analysis of genetic distance reveals relationships between the populations that are similar to their geographical arrangement. A strong negative correlation exists between the level of heterozygosity within island populations of C. nusatenggara and the minimum sea-crossing distance to the nearest large source population. This is interpreted as reflecting an isolation effect of the sea, leading to reduced heterozygosity in populations that have larger sea barriers between them and the large source islands. Independently of this, heterozygosity is negatively associated with longitude, which in turn is associated with systematic changes in the environment such as a gradual decline in rainfall from west to east. The association between heterozygosity and longitude is interpreted as reflecting an association between genetic and environmental variance and supports the niche-width theory of genetic variance. Morphometric variability did not show any of the main effects demonstrated in the genetic data. Furthermore, there was no evidence that, at the level of individuals, genetic and morphometric variability were associated.     

QUANTITATIVE GENETICS OF BRYOZOAN PHENOTYPIC EVOLUTION. II. ANALYSIS OF SELECTION AND RANDOM CHANGE IN FOSSIL SPECIES USING RECONSTRUCTED GENETIC PARAMETERS

The roles of natural selection and random genetic change in the punctuated phenotypic evolution of eight Miocene-Pliocene tropical American species of the cheilostome bryozoan Metrarabdotos are analyzed by quantitative genetic methods. Trait heritabilities and genetic covariances reconstructed by partitioning within- and among-colony phenotypic variance are similar to those previously obtained for living species of the cheilostome Stylopoma using breeding data. The hypothesis that differences in skeletal morphology between species of Metrarabdotos are entirely due to mutation and genetic drift cannot be rejected for reasonable rates of mutation maintained for periods brief enough to account for the geologically abrupt appearances of these species in the fossil record. Except for one pair of species, separated by the largest morphologic distance, directional selection acting alone would require unrealistically high rates of selective mortality to be maintained for these periods. Thus, directional selection is not strongly implicated in the divergence of Metrarabdotos species. Within species, rates of net phenotypic change are slow enough to require stabilizing selection, but mask large, relatively rapid fluctuations, all of which, however, can be attributed to chance departures from the mean phenotype by mutation and genetic drift, rather than to tracking environmental fluctuation by directional selection. The results are consistent with genetic models involving shifts between multiple adaptive peaks on which phenotypes remain more or less static through long-term stabilizing selection. Regardless of the degree to which directional selection may be involved in peak shifts, phenotypic differentiation is thus related to processes different than the pervasive stabilizing selection acting within species.     

GENETIC CONSTRAINTS ON MACROEVOLUTION: THE EVOLUTION OF HOST AFFILIATION IN THE LEAF BEETLE GENUS OPHRAELLA

We hypothesize that the evolution of an ecologically important character, the host associations of specialized phytophagous insects, has been influenced by limitations on genetic variation. Using as a historical framework a phylogenetic reconstruction of the history of host associations in the beetle genus Ophraella (Chrysomelidae), we have employed quantitative-genetic methods to screen four species for genetic variation in larval survival, oviposition (in one species only), and feeding responses to their congeners' host plants, in the Asteraceae. We here report results of studies of one species and evaluate the results from all four. Analysis of half-sib/full-sib families and of progenies of wild females of O. notulata, a specialist on Iva (Ambrosiinae), provided evidence of genetic variation in larval consumption of five of six test plants and in adult consumption of four of six. Larval mortality was complete on five plants; only on Ambrosia, a close relative of the natural host, was there appreciable, and genetically variable, survival. Oviposition on Ambrosia showed marginally significant evidence of genetic variation; a more distantly related plant elicited no oviposition at all. In compiling results from four Ophraella species, reported in this and two other papers, we found no evidence of genetic variation in 18 of 39 tests of feeding responses and 14 of 16 tests of larval survival on congeners' hosts. This result is consistent with the hypothesis that absence or paucity of genetic variation may constrain or at least bias the evolution of host associations. The lower incidence of genetic variation in survival than in feeding behavior may imply, according to recent models, that avoidance is a more common evolutionary response to novel plants than adaptation. The usually great disparity between mean performance on congeners' hosts and the species' natural hosts, and an almost complete lack of evidence for negative genetic correlations, argue against the likelihood that speciation has occurred by sympatric host shift. The presence versus apparent absence of genetic variation in consumption was correlated with the propinquity of relationship between the beetle species tested and the species that normally feeds on the test plant, suggesting that the history of host shifts in Ophraella has been guided in part by restrictions on genetic variation. It was also correlated with the propinquity of relationship between a test plant and the beetle's natural host. The contributions of plant relationships and insect relationships, themselves correlated in part, to the pattern of genetic variation, are not readily distinguishable, but together accord with phylogenetic evidence that these and other phytophagous insects adapt most readily to related plants. In this instance, therefore, the macroevolution of an ecologically important character appears to have been influenced by genetic constraints. We hypothesize that absence of the structural prerequisites for genetic variation in complex characters may affect genetic variation and the trajectory of evolution.     

DIFFERENTIAL DOMINANCE OF PLEIOTROPIC LOCI FOR MOUSE SKELETAL TRAITS

The term "differential dominance" describes the situation in which the dominance effects at a pleiotropic locus vary between traits. Directional selection on the phenotype can lead to balancing selection on differentially dominant pleiotropic loci. Even without any individual overdominant traits, some linear combination of traits will display overdominance at a locus displaying differential dominance. Multivariate overdominance may be responsible, in part, for high levels of heterozygosity found in natural populations. We examine differential dominance of 70 mouse skeletal traits at 92 quantitative trait loci (QTL). Our results indicate moderate to strong additive and dominance effects at pleiotropic loci, low levels of individual-trait overdominance, and universal multivariate overdominance. Multivariate overdominance affects a range of 6% to 81% of morphospace, with a mean of 32%. Multivariate overdominance tends to affect a larger percentage of morphospace at pleiotropic loci with antagonistic effects on multiple traits (42%). We conclude that multivariate overdominance is common and should be considered in models and in empirical studies of the role of genetic variation in evolvability.     

GENETIC COVARIANCE OF FITNESS CORRELATES: WHAT GENETIC CORRELATIONS ARE MADE OF AND WHY IT MATTERS

The genetic variance-covariance matrix, G, is determined in part by functional architecture, the pathways by which variation in genotype influences phenotype. I develop a simple architectural model for G for two traits under directional selection constrained by their dependence on a common limiting resource. I assume that genetic variance is maintained by mutation-selection balance. The relative numbers of loci that play a role in acquiring versus allocating a limiting resource play a crucial role in determining genetic covariance. If many loci are involved in acquiring a resource, genetic covariance may be either negative or positive at equilibrium, depending on the fitness function and the input of mutational variance. The form of G does not necessarily reveal the constraint on resource acquisition inherent in the system, and therefore studies estimating G do not test for the existence of life-history tradeoffs. Characters may evolve in patterns that are unpredictable from G. Experiments are suggested that would indicate if this model could explain observations of positive genetic covariance.     

INTERACTING PHENOTYPES AND THE EVOLUTIONARY PROCESS: I. DIRECT AND INDIRECT GENETIC EFFECTS OF SOCIAL INTERACTIONS

Interacting phenotypes are traits whose expression is affected by interactions with conspecifics. Commonly-studied interacting phenotypes include aggression, courtship, and communication. More extreme examples of interacting phenotypes—traits that exist exclusively as a product of interactions—include social dominance, intraspecific competitive ability, and mating systems. We adopt a quantitative genetic approach to assess genetic influences on interacting phenotypes. We partition genetic and environmental effects so that traits in conspecifics that influence the expression of interacting phenotypes are a component of the environment. When the trait having the effect is heritable, the environmental influence arising from the interaction has a genetic basis and can be incorporated as an indirect genetic effect. However, because it has a genetic basis, this environmental component can evolve. Therefore, to consider the evolution of interacting phenotypes we simultaneously consider changes in the direct genetic contributions to a trait (as a standard quantitative genetic approach would evaluate) as well as changes in the environmental (indirect genetic) contribution to the phenotype. We then explore the ramifications of this model of inheritance on the evolution of interacting phenotypes. The relative rate of evolution in interacting phenotypes can be quite different from that predicted by a standard quantitative genetic analysis. Phenotypic evolution is greatly enhanced or inhibited depending on the nature of the direct and indirect genetic effects. Further, unlike most models of phenotypic evolution, a lack of variation in direct genetic effects does not preclude evolution if there is genetic variance in the indirect genetic contributions. The available empirical evidence regarding the evolution of behavior expressed in interactions, although limited, supports the predictions of our model.     

SMALL POPULATION GENETIC VARIABILITY AT LOCI UNDER STABILIZING SELECTION

Genetic variability at a locus under stabilizing selection in a finite population is investigated using analytic methods and computer simulations. Three measures are examined: the number of alleles k, heterozygosity H, and additive genetic variance Vg. A nearly-neutral theory results. The composite parameter S = NV_M/V_s (where N is the population size, V_M the variance of new mutant allelic effects and V_s the weakness of stabilizing selection) figures prominently in the results. The equilibrium heterozygosity is similar to that of strictly neutral theory, H = 4N_μc/ (1 + 4N_μc), except that μ_c = where c is about 0.5. Simulations corroborate except for very low N. Genetic variability attains similar equilibrium values at both a “lone” locus and at an “embedded” locus. This agrees with my earlier work concerning molecular clock rates. These results modify the neutralist interpretation of data concerning genetic variability and genetic distances between populations. Low H values are proportional not to N but to . This may explain the narrow observed range of H among species. Heterozygosities need not be highly correlated to genetic variances. Genetic variances are not highly dependent on population size except in very small populations which are difficult to sample without bias because the smallest populations go extinct the fastest. Nearly neutral evolution will not be easily distinguished from strictly neutral theory under the Hudson-Kreitman-Aguade inter-/intraspecific variation ratio test, since a similar effective mutation rate holds for genetic distances and D = 2μ_ct, where . As with strictly neutral theory, comparisons across loci should show D and H to be positively correlated because of the shared μ_c. But unlike neutral theory, for a given locus, comparisons across species should show D and H to be negatively correlated. There is no obvious threshold of population size below which genetic variability inevitably declines. Extinction depends on both genetic variation and natural selection. Neither theory nor observation presently indicates the measure of genetic variability (k, H, V_G or other) that best indicates vulnerability of a small population to extinction.     

THE QUANTITATIVE AND MOLECULAR GENETIC ARCHITECTURE OF A SUBDIVIDED SPECIES

In an effort to elucidate the evolutionary mechanisms that determine the genetic architecture of a species, we have analyzed 17 populations of the microcrustacean Daphnia pulex for levels of genetic variation at the level of life-history characters and molecular markers in the nuclear and mitochondrial genomes. This species is highly subdivided, with approximately 30% of the variation for nuclear molecular markers and 50% of the variation for mitochondrial markers being distributed among populations. The average level of genetic subdivision for quantitative traits is essentially the same as that for nuclear markers, which superficially suggests that the life-history characters are diverging at the neutral rate. However, the existence of a strong correlation between the levels of population subdivision and broadsense heritabilities of individual traits argues against this interpretation, suggesting instead that the among-population divergence of some quantitative traits (most notably body size) is being driven by local adaptation to different environments. The fact that the mean phenotypes of the individual populations are also strongly correlated with local levels of homozygosity indicates that variation in local inbreeding plays a role in population differentiation. Rather than being a passive consequence of local founder effects, levels of homozygosity may be selected for directly for their effects on the phenotype (adaptive inbreeding depression). There is no relationship between the levels of variation within populations for molecular markers and quantitative characters, and this is explained by the fact that the average standing genetic variation for life-history characters in this species is equivalent to only 33 generations of variation generated by mutation.     

SEX-SPECIFIC GENETIC VARIANCE AND THE EVOLUTION OF SEXUAL DIMORPHISM: A SYSTEMATIC REVIEW OF CROSS-SEX GENETIC CORRELATIONS

The independent evolution of the sexes may often be constrained if male and female homologous traits share a similar genetic architecture. Thus, cross-sex genetic covariance is assumed to play a key role in the evolution of sexual dimorphism (SD) with consequent impacts on sexual selection, population dynamics, and speciation processes. We compiled cross-sex genetic correlations ( r _MF) estimates from 114 sources to assess the extent to which the evolution of SD is typically constrained and test several specific hypotheses. First, we tested if r _MF differed among trait types and especially between fitness components and other traits. We also tested the theoretical prediction of a negative relationship between r _MF and SD based on the expectation that increases in SD should be facilitated by sex-specific genetic variance. We show that r _MF is usually large and positive but that it is typically smaller for fitness components. This demonstrates that the evolution of SD is typically genetically constrained and that sex-specific selection coefficients may often be opposite in sign due to sub-optimal levels of SD. Most importantly, we confirm that sex-specific genetic variance is an important contributor to the evolution of SD by validating the prediction of a negative correlation between r _MF and SD.     

PERSPECTIVE: COMPLEX ADAPTATIONS AND THE EVOLUTION OF EVOLVABILITY

The problem of complex adaptations is studied in two largely disconnected research traditions: evolutionary biology and evolutionary computer science. This paper summarizes the results from both areas and compares their implications. In evolutionary computer science it was found that the Darwinian process of mutation, recombination and selection is not universally effective in improving complex systems like computer programs or chip designs. For adaptation to occur, these systems must possess “evolvability,” i.e., the ability of random variations to sometimes produce improvement. It was found that evolvability critically depends on the way genetic variation maps onto phenotypic variation, an issue known as the representation problem. The genotype-phenotype map determines the variability of characters, which is the propensity to vary. Variability needs to be distinguished from variations, which are the actually realized differences between individuals. The genotype-phenotype map is the common theme underlying such varied biological phenomena as genetic canalization, developmental constraints, biological versatility, developmental dissociability, and morphological integration. For evolutionary biology the representation problem has important implications: how is it that extant species acquired a genotype-phenotype map which allows improvement by mutation and selection? Is the genotype-phenotype map able to change in evolution? What are the selective forces, if any, that shape the genotype-phenotype map? We propose that the genotype-phenotype map can evolve by two main routes: epistatic mutations, or the creation of new genes. A common result for organismic design is modularity. By modularity we mean a genotype-phenotype map in which there are few pleiotropic effects among characters serving different functions, with pleiotropic effects falling mainly among characters that are part of a single functional complex. Such a design is expected to improve evolvability by limiting the interference between the adaptation of different functions. Several population genetic models are reviewed that are intended to explain the evolutionary origin of a modular design. While our current knowledge is insufficient to assess the plausibility of these models, they form the beginning of a framework for understanding the evolution of the genotype-phenotype map.     

THE EVOLUTION OF CANALIZATION AND THE BREAKING OF VON BAER'S LAWS: MODELING THE EVOLUTION OF DEVELOPMENT WITH EPISTASIS

Evolution can change the developmental processes underlying a character without changing the average expression of the character itself. This sort of change must occur in both the evolution of canalization, in which a character becomes increasingly buffered against genetic or developmental variation, and in the phenomenon of closely related species that show similar adult phenotypes but different underlying developmental patterns. To study such phenomena, I develop a model that follows evolution on a surface representing adult phenotype as a function of underlying developmental characters. A contour on such a “phenotype landscape” is a set of states of developmental characters that produce the same adult phenotype. Epistasis induces curvature of this surface, and degree of canalization is represented by the slope along a contour. I first discuss the geometric properties of phenotype landscapes, relating epistasis to canalization. I then impose a fitness function on the phenotype and model evolution of developmental characters as a function of the fitness function and the local geometry of the surface. This model shows how canalization evolves as a population approaches an optimum phenotype. It further shows that under some circumstances, “decanalization” can occur, in which the expression of adult phenotype becomes increasingly sensitive to developmental variation. This process can cause very similar populations to diverge from one another developmentally even when their adult phenotypes experience identical selection regimes.     

ON THE EVOLUTION OF PHENOTYPIC PLASTICITY IN A SPATIALLY HETEROGENEOUS ENVIRONMENT

A genetic model for the dynamics of a quantitative trait is analyzed in terms of gene frequencies, linkage disequilibria, and environmental effects on the trait. In a randomly mating population, at each generation progeny move to niches where they are subject to weak Gaussian selection on the trait, with different fitness levels in the different niches. Initially, the variability of the trait is due to additive loci with heterozygous homeostasis. The evolution of plasticity is then described in terms of the invasion of the population by genetic modifiers that may epistatically affect the trait, its optimum in each niche, the strengths of selection, and other parameters characteristic of the niches. We show that the evolution of trait means within niches depends on the overall evolution in the whole system, and in general, optimum phenotypic values are not attained. The reaction norm and genotype-environment interaction may evolve even if the only effects of the modifier are on individual rates of dispersal, or on fitness effects resulting from the different environments in the different niches; this evolution does not require that the modifier affect parameters that influence the values of the trait. It is conjectured that in the least frequently reached niches with low fitness levels, the deviations from the trait optima should be larger than those in more commonly experienced and less stringent niches. Our analysis makes explicit the different contribution of between- and within-niche effects on the evolutionary dynamics of phenotypic plasticity in heterogeneous environments.     

SEXUAL CONFLICT AND THE MAINTENANCE OF MULTIVARIATE GENETIC VARIATION

Mate choice should erode additive genetic variation in sexual displays, yet these traits often harbor substantial genetic variation. Nevertheless, recent developments in quantitative genetics have suggested that multivariate genetic variation in the combinations of traits under selection may still be depleted. Accordingly, the erosion and maintenance of variation may only be detectable by studying whole suites of traits. One potential process favoring the maintenance of genetic variance in multiple trait combinations is the modification of sexual selection via sexually antagonistic interactions between males and females. Here we consider how interlocus sexual conflict can shape the genetic architecture of male sexual traits in the cricket, Teleogryllus commodus. In this species, the ability of each sex to manipulate insemination success significantly alters the selection acting on male courtship call properties. Using a quantitative genetic breeding design we estimated the additive genetic variation in these traits and then predicted the change in variation due to previously documented patterns of sexual selection. Our results indicate that female choice should indeed deplete multivariate genetic variance, but that sexual conflict over insemination success may oppose this loss of variance. We suggest that changes in the direction of selection due to sexually antagonistic interactions will be an important and potentially widespread factor in maintaining multivariate genetic variation.     

GENERALISTS,SPECIALISTS, AND THE EVOLUTION OF PHENOTYPIC PLASTICITY IN SYMPATRIC POPULATIONS OF DISTINCT SPECIES

The evolution of phenotypic plasticity is studied in a model with two reproductively isolated “species” in a coarse-grained environment, consisting of two types of habitats. A quantitative genetic model for selection was constructed, in which habitats differ in the optimal value for a focal trait, and with random dispersal among habitats. The main interest was to study the effects of different selection regimes. Three cases were investigated: (1) without any limits to plasticity; (2) without genetic variation for plasticity; and (3) with a fitness cost for phenotypically plastic reactions. In almost all cases a generalist strategy to exploit both habitats emerged. Without any limits to plasticity, optimal adaptive reactions evolved. Without any genetic variation for plasticity, a compromise strategy with an intermediate, fixed phenotype evolved, whereas in the presence of costs a plastic compromise between the demands of the habitats and the costs associated with plasticity was found. Specialization and phenotypic differentiation was only found when selection within habitats was severe and optimal phenotypes for different habitats were widely different. Under soft selection (local regulation of population numbers in each habitat) the specialists coexisted; under hard selection (global regulation of population numbers) one specialist outcompeted the other. The prevalent evolutionary outcome of compromises rather than specialization implies that costs or constraints are not necessarily detectable as local adaptation in transplantation or translocation experiments.