Ecology and evolution of symbiosis in metapopulations

We present a model for symbionts in plant host metapopulation. Symbionts are assumed not only to form a systemic infection throughout the host and pass into the host seeds, but also to reproduce and infect new plants by spores. Thus, we study a metapopulation of qualitatively identical patches coupled through seeds and spores dispersal. Symbionts that are only vertically inherited cannot persist in such a uniform environment if they lower the host's fitness. They have to be beneficial in order to coexist with the host if they are not perfectly transmitted to the seeds; but evolution selects for 100% fidelity of infection inheritance. In this model we want to see how mixed strategies (both vertical and horizontal infection) affect the coexistence of uninfected and infected plants at equilibrium; also, what would evolution do for the host, for the symbionts and for their association. We present a detailed classification of the possible equilibria with examples. The stability of the steady states is rigorously proved for the first time in a metapopulation set-up.     

Ecology and evolution of symbiosis in metapopulations

We present a model for symbionts in plant host metapopulation. Symbionts are assumed not only to form a systemic infection throughout the host and pass into the host seeds, but also to reproduce and infect new plants by spores. Thus, we study a metapopulation of qualitatively identical patches coupled through seeds and spores dispersal. Symbionts that are only vertically inherited cannot persist in such a uniform environment if they lower the host's fitness. They have to be beneficial in order to coexist with the host if they are not perfectly transmitted to the seeds; but evolution selects for 100% fidelity of infection inheritance. In this model we want to see how mixed strategies (both vertical and horizontal infection) affect the coexistence of uninfected and infected plants at equilibrium; also, what would evolution do for the host, for the symbionts and for their association. We present a detailed classification of the possible equilibria with examples. The stability of the steady states is rigorously proved for the first time in a metapopulation set-up.     

Joint evolution of specialization and dispersal in structured metapopulations

We study the joint evolution of dispersal and specialization concerning resource usage in a mechanistically underpinned structured discrete-time metapopulation model. We show that dispersal significantly affects the evolution of specialization and that specialization is a key factor that determines the possibility of evolutionary branching in dispersal propensity. Allowing both dispersal propensity and specialization to evolve as a consequence of natural selection is necessary in order to understand the evolutionary dynamics. The joint evolution of dispersal and specialization forms a natural evolutionary path leading to the coexistence of generalists and specialists. We show that in this process, the number of different patch types and the resource distribution are essential.     

Evolutionary suicide and evolution of dispersal in structured metapopulations

 We study the evolution of dispersal in a structured metapopulation model. The metapopulation consists of a large (infinite) number of local populations living in patches of habitable environment. Dispersal between patches is modelled by a disperser pool and individuals in transit between patches are exposed to a risk of mortality. Occasionally, local catastrophes eradicate a local population: all individuals in the affected patch die, yet the patch remains habitable. We prove that, in the absence of catastrophes, the strategy not to migrate is evolutionarily stable. Under a given set of environmental conditions, a metapopulation may be viable and yet selection may favor dispersal rates that drive the metapopulation to extinction. This phenomenon is known as evolutionary suicide. We show that in our model evolutionary suicide can occur for catastrophe rates that increase with decreasing local population size. Evolutionary suicide can also happen for constant catastrophe rates, if local growth within patches shows an Allee effect. We study the evolutionary bifurcation towards evolutionary suicide and show that a discontinuous transition to extinction is a necessary condition for evolutionary suicide to occur. In other words, if population size smoothly approaches zero at a boundary of viability in parameter space, this boundary is evolutionarily repelling and no suicide can occur. Received: 10 November 2000 / Revised version: 13 February 2002 / Published online: 17 July 2002     

On the evolution of specialization with a mechanistic underpinning in structured metapopulations

We analyze the evolution of specialization in resource utilization in a discrete-time metapopulation model using the adaptive dynamics approach. The local dynamics in the metapopulation are based on the Beverton-Holt model with mechanistic underpinnings. The consumer faces a trade-off in the abilities to consume two resources that are spatially heterogeneously distributed to patches that are prone to local catastrophes. We explore the factors favoring the spread of generalist or specialist strategies. Increasing fecundity or decreasing catastrophe probability favors the spread of the generalist strategy and increasing environmental heterogeneity enlarges the parameter domain where the evolutionary branching is possible. When there are no catastrophes, increasing emigration diminishes the parameter domain where the evolutionary branching may occur. Otherwise, the effect of emigration on evolutionary dynamics is non-monotonous: both small and large values of emigration probability favor the spread of the specialist strategies whereas the parameter domain where evolutionary branching may occur is largest when the emigration probability has intermediate values. We compare how different forms of spatial heterogeneity and different models of local growth affect the evolutionary dynamics. We show that even small changes in the resource dynamics may have outstanding evolutionary effects to the consumers.     

Antler size in red deer: heritability and selection but no evolution

We present estimates of the selection on and the heritability of a male secondary sexual weapon in a wild population: antler size in red deer. Male red deer with large antlers had increased lifetime breeding success, both before and after correcting for body size, generating a standardized selection gradient of 0.44 (+/- 0.18 SE). Despite substantial age- and environment-related variation, antler size was also heritable (heritability of antler mass = 0.33 +/- 0.12). However the observed selection did not generate an evolutionary response in antler size over the study period of nearly 30 years, and there was no evidence of a positive genetic correlation between antler size and fitness nor of a positive association between breeding values for antler size and fitness. Our results are consistent with the hypothesis that a heritable trait under directional selection will not evolve if associations between the measured trait and fitness are determined by environmental covariances: In red deer males, for example, both antler size and success in the fights for mates may be heavily dependent on an individual's nutritional state.     

The heritability of insomnia: A meta-analysis of twin studies

Twin studies of insomnia exhibit heterogeneity in estimates of heritability. This heterogeneity is likely because of sex differences, age of the sample, the reporter and the definition of insomnia. The aim of the present study was to systematically search the literature for twin studies investigating insomnia disorder and insomnia symptoms and to meta-analyse the estimates of heritability derived from these studies to generate an overall estimate of heritability. We further examined whether heritability was moderated by sex, age, reporter and insomnia symptom. A systematic literature search of five online databases was completed on 24 January 2020. Two authors independently screened 5644 abstracts, and 160 complete papers for the inclusion criteria of twin studies from the general population reporting heritability statistics on insomnia or insomnia symptoms, written in English, reporting data from independent studies. We ultimately included 12 papers in the meta-analysis. The meta-analysis focussed on twin intra-class correlations for monozygotic and dizygotic twins. Based on these intra-class correlations, the meta-analytic estimate of heritability was estimated at 40%. Moderator analyses showed stronger heritability in females than males; and for parent-reported insomnia symptoms compared with self-reported insomnia symptoms. There were no other significant moderator effects, although this is likely because of the small number of studies that were comparable across levels of the moderators. Our meta-analysis provides a robust estimate of the heritability of insomnia, which can inform future research aiming to uncover molecular genetic factors involved in insomnia vulnerability.     

Environmental coupling of selection and heritability limits evolution

There has recently been great interest in applying theoretical quantitative genetic models to empirical studies of evolution in wild populations. However, while classical models assume environmental constancy, most natural populations exist in variable environments. Here, we applied a novel analytical technique to a long-term study of birthweight in wild sheep and examined, for the first time, how variation in environmental quality simultaneously influences the strength of natural selection and the genetic basis of trait variability. In addition to demonstrating that selection and genetic variance vary dramatically across environments, our results show that environmental heterogeneity induces a negative correlation between these two parameters. Harsh environmental conditions were associated with strong selection for increased birthweight but low genetic variance, and vice versa. Consequently, the potential for microevolution in this population is constrained by either a lack of heritable variation (in poor environments) or by a reduced strength of selection (in good environments). More generally, environmental dependence of this nature may act to limit rates of evolution, maintain genetic variance, and favour phenotypic stasis in many natural systems. Assumptions of environmental constancy are likely to be violated in natural systems, and failure to acknowledge this may generate highly misleading expectations for phenotypic microevolution.     

Connectivity and resilience of coral reef metapopulations in marine protected areas: matching empirical efforts to predictive needs

Design and decision-making for marine protected areas (MPAs) on coral reefs require prediction of MPA effects with population models. Modeling of MPAs has shown how the persistence of metapopulations in systems of MPAs depends on the size and spacing of MPAs, and levels of fishing outside the MPAs. However, the pattern of demographic connectivity produced by larval dispersal is a key uncertainty in those modeling studies. The information required to assess population persistence is a dispersal matrix containing the fraction of larvae traveling to each location from each location, not just the current number of larvae exchanged among locations. Recent metapopulation modeling research with hypothetical dispersal matrices has shown how the spatial scale of dispersal, degree of advection versus diffusion, total larval output, and temporal and spatial variability in dispersal influence population persistence. Recent empirical studies using population genetics, parentage analysis, and geochemical and artificial marks in calcified structures have improved the understanding of dispersal. However, many such studies report current self-recruitment (locally produced settlement/settlement from elsewhere), which is not as directly useful as local retention (locally produced settlement/total locally released), which is a component of the dispersal matrix. Modeling of biophysical circulation with larval particle tracking can provide the required elements of dispersal matrices and assess their sensitivity to flows and larval behavior, but it requires more assumptions than direct empirical methods. To make rapid progress in understanding the scales and patterns of connectivity, greater communication between empiricists and population modelers will be needed. Empiricists need to focus more on identifying the characteristics of the dispersal matrix, while population modelers need to track and assimilate evolving empirical results.     

Genome-wide association studies in plants: the missing heritability is in the field

Genome-wide association studies (GWAS) have been even more successful in plants than in humans. Mapping approaches can be extended to dissect adaptive genetic variation from structured background variation in an ecological context.     

Chromatin and heritability: how epigenetic studies can complement genetic approaches

Despite the success in using genome-wide association studies to identify many loci associated with human disease, there are several gaps in understanding of how common genetic diseases are manifested. Epigenetic studies, which focus on DNA and chromatin modifications, have the potential to complement genetic approaches and provide more insight into mechanism, environmental effects and modes of inheritance, including the potential for non-DNA-based heritability. However, there are considerable challenges in designing and interpreting epigenetic studies associated with disease. Here, I review recent studies focused on individual variation in chromatin, and outline how epigenome-based studies can be used to complement genetic studies. In particular, I see more benefit to epigenetic studies being performed in the context of genetic studies, rather than as separate investigations.     

Interspecific competition in metapopulations

The assumptions and predictions of metapopulation models for competing species are discussed in relation to empirical studies of colonization and extinction in metapopulations. In three species of Daphnia in rockpools, interspecific competition increased local extinction rates, while no effects on colonization rates were detected. Distributional patterns were consistent with several predictions of the competition model; for example, the number of species on an island increased with the number of pools and the proportion of pools occupied by each species decreased with increasing species number. It is concluded that interspecific competition is important for the distributional dynamics of Daphnia species in rockpools, but the question whether the coexistence of these species depends on metapopulation dynamics is still unresolved. Other studies on the effects of interspecific competition on colonization and extinction rates are discussed.     

Null models of geographic range size evolution reaffirm its heritability

Most models of allopatric speciation predict that the two daughter species will have range sizes different from each other's and potentially from that of their common ancestor. However, I find that this difference is less than that expected under a variety of null models of range evolution. Sister species' range values may therefore become more similar in the time following speciation. Greater-than-expected similarity (symmetry) has also been treated as a form of range size heritability. I therefore compare the results of this symmetry approach to a test for phylogenetic signal, using the range sizes of North American birds. I find that range size is heritable under both tests. I suggest that null models for range size heritability should be informed by an explicit model of evolution. Comparative methods may give erroneous results if they fail to take the unusual form of inheritance of range size into account.     

Laboratory evolution of adenylyl cyclase independent learning in Drosophila and missing heritability

Gene interactions are acknowledged to be a likely source of missing heritability in large‐scale genetic studies of complex neurological phenotypes. However, involvement of rare variants, de novo mutations, genetic lesions that are not easily detected with commonly used methods and epigenetic factors also are possible explanations. We used a laboratory evolution study to investigate the modulatory effects of background genetic variation on the phenotypic effect size of a null mutation with known impact on olfactory learning. To accomplish this, we first established a population that contained variation at just 23 loci and used selection to evolve suppression of the learning defect seen with null mutations in the rutabaga adenylyl cyclase. We thus biased the system to favor relatively simplified outcomes by choosing a Mendelian trait and by restricting the genetic variation segregating in the population. This experimental design also assures that the causal effects are among the known 23 segregating loci. We observe a robust response to selection that requires the presence of the 23 variants. Analyses of the underlying genotypes showed that interactions between more than two loci are likely to be involved in explaining the selection response, with implications for the missing heritability problem.     

The population ecology of contemporary adaptations: what empirical studies reveal about the conditions that promote adaptive evolution

Genetica - Under what conditions might organisms be capable of rapid adaptive evolution? We reviewed published studies documenting contemporary adaptations in natural populations and looked for...     

Ecological and Populational Developmental Biology: There and Back

Russian Journal of Developmental Biology -     

Estimating missing heritability for disease from genome-wide association studies

Genome-wide association studies are designed to discover SNPs that are associated with a complex trait. Employing strict significance thresholds when testing individual SNPs avoids false positives at the expense of increasing false negatives. Recently, we developed a method for quantitative traits that estimates the variation accounted for when fitting all SNPs simultaneously. Here we develop this method further for case-control studies. We use a linear mixed model for analysis of binary traits and transform the estimates to a liability scale by adjusting both for scale and for ascertainment of the case samples. We show by theory and simulation that the method is unbiased. We apply the method to data from the Wellcome Trust Case Control Consortium and show that a substantial proportion of variation in liability for Crohn disease, bipolar disorder, and type I diabetes is tagged by common SNPs.