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The first section of this chapter presents new theory showing that sex-specific patterns of genomic imprinting may play a role in the genetic architecture and expression of sexually dimorphic traits. Empirical evidence tentatively supports this novel theory. The second section considers the potential role of condition dependence in the evolution of sexual dimorphism. Life history theory predicts that sexual dimorphism and condition dependence will co-evolve because the degree of exaggeration of male secondary sexual traits by sexual selection is expected to reflect the viability costs of trait expression and, therefore, the benefits of condition dependence. This prediction is supported by positive covariation of sexual dimorphism and condition dependence among morphological traits. Condition dependence of male traits is also expected to reduce intersexual genetic correlations, and thus mitigate intralocus sexual conflict and facilitate the evolution of sexual dimorphism.

Basic and applied research programs can both benefit by approaching concerns regarding resistance to herbivores from a perspective centering on natural selection and genetic architecture of resistance. In natural systems, quantification of selection, determination of genetic correlations with other traits, and evaluation of genetic architecture can enhance our ability to predict the evolution of plant resistance. This chapter explores the selective agents that influence plant resistance to insect herbivores, the strength of selection, and the genetic architecture of resistance traits. It also discusses the relationship between plant hybrid resistance and the resistance of parental populations or species, which have implications for hybrid zone dynamics and for introgression of resistance traits between populations or species. Moreover, the chapter looks at the trade-offs between resistance and tolerance, allocation costs to resistance, ecological costs to resistance, potential impacts of hybridization, and the architecture of resistance in willows Salix eriocephala and Salix sericea.

The complexity of biological systems often prevents the construction of deterministic framework for the relationship between genotypes and phenotypes in development and evolution. The void is filled by the field of epigenetics that studies properties of emergent, self-regulatory, and compensatory interactions that arise above the level of the gene, but are not directly predictable from the intrinsic properties of either phenotype or genotype. Although these interactions are ubiquitous in the development and functioning of phenotypes, their imprint on the evolution of genetic architecture is unclear. This chapter particularly addresses the contribution of epigenetic developmental dynamics to the maintenance of multivariate genetic variation in complex traits that are subject to strong natural selection. The chapter brings together geometric and developmental perspectives to understanding the evolution of genetic architecture that reconciles precise adaptation, evolutionary diversification, and environmentally contingent developmental variation.

This chapter takes a deeper look into the genetics of both the host and the parasite. First, it explores the genetic architecture of host resistance, as well as several methods that are used to elucidate genetic architecture – such as QTL-analysis, gene sequencing, comparative genetic studies, and quantitative genetics. The analyses suggest that host resistance is often based upon a limited number of genes with major effect. The genetics of parasite virulence, on the other hand, is illustrated by bacterial pathogens. The chapter indicates that pathogenicity islands are where importance virulence genes are often located. These pathogenicity islands have their own life-cycle, during which they are transferred to a new host, become adapted, and eventually might be excised and transferred again to a further line. The chapter furthermore explores variation in gene expression, which is also a major source of differences in host–parasite interactions.

Most phenotypic traits are the product of many genes as well as environmental effects, and the resulting phenotypic variation is quantitative rather than qualitative. The extent to which traits are under genetic control is termed heritability, and can be estimated by analyzing the phenotypic similarity of related individuals. Quantitative genetic approaches can be used to estimate population differentiation. Selection on quantitative traits produces changes in phenotypes as a function of the heritability, the intensity of selection, and the amount of phenotypic variation within a population. Human activities, such as size-limited harvesting and habitat degradation, can impose selection on natural populations and result in changes in phenotypes, and genetic drift in small populations can erode quantitative genetic variation. Genome-wide association studies can identify genes and markers associated with quantitative trait variation that can then be used to predict phenotypes from polygenic scores.

Heliconius wing patterns have been the focus of evolutionary genetic analysis for many years. Early genetic studies characterized a large number of Mendelian loci with large effects on wing pattern elements. The recent application of molecular genetic markers has led to recognition that a huge range of allelic variation at just four major loci controls most of the Heliconius radiation. Some of these loci consist of tightly linked components that can be separated by occasional recombination. More recent quantitative analyses has also identified minor effect loci that influence the expression of these major loci. A single locus polymorphism in Heliconius numata provides an example of a ‘supergene’, in which a single major locus controls segregation of a variable phenotype. Inversion polymorphisms are associated with wing pattern variation in wild populations, which reduce recombination across the supergene locus. This provides evidence that the architecture and organization of genomes can be shaped by natural selection.

The genotype is that part of the genetic make-up of an organism causally responsible, to greater or lesser degrees, for the phenotype. The underlying genetic basis of a trait depends on genetic architecture; phenotypic differences can be caused by many genes, each having a small effect, and/or few genes each having a large effect. Some traits are influenced by groups of many genes linked together on the same chromosome and inherited as single units or supergenes. A particular type of genetic variation (additive genetic variance) determines trait heritability, i.e. the similarity in trait phenotype between parents and offspring. Trait heritability and genetic trade-offs influence the response of traits to natural and human-induced selection. A key point is that genes rarely act in isolation of one another, rendering it challenging to reliably predict evolutionary responses to selection. Thereafter, following a section on how the environment can affect the phenotypically plastic expression of traits, the chapter explores genotype-by-environment interactions, using reaction norms. These are visually heuristic and intuitively tractable depictions of how a trait varies with an environmental factor or with another trait. Reaction norms have long been used to study phenotypic plasticity. Today, they are increasingly seen as an invaluable tool for examining genetic differences in how individuals and populations respond to environmental change.

Most phenotypic traits are affected by a multitude of genes, which may interact in complex ways. This means that the single locus model explored in chapters 3 and 4 is not always able to capture the full complexity of genetic evolution. In many cases, multiple genes are involved and so this chapter formalizes the analysis of multilocus evolution. Concepts such as linkage disequilibrium and epistasis are introduced, both of which are necessary to properly understand multilocus evolution. The currently highly active field emerging as a result of a crossover between quantitative genetics and genomics is further explored, including methods such as quantitative trait locus (QTL) analysis and genome wide association study (GWAS) that allow phenotypic variation to be associated with likely causative genes and that have made important advances in our understanding of the genetic underpinnings of disease.

In a large population in the absence of new mutation, selection is expected to eventually drive all of the additive-genetic variance in a trait toward zero, resulting in a selection limit. This chapter examines the underlying population-genetics of such a limit, how it is estimated, and reviews the actual nature of limits observed in artificial selection experiments. It also examines the conditions under which a major gene is more important than polygenic response.

More than 200 years after the discovery of floral mimicry by Sprengel many questions about this fascinating natural phenomenon remain unanswered. Floral mimicry has traditionally been a relatively small field of research compared with animal mimicry; however, floral mimicry studies now account for almost a third of all studies dealing with mimicry among organisms. This chapter looks to the future of mimicry research and focuses on molecular approaches and their potential to answer unresolved questions about speciation. The inclusion of this chapter does not mean that the future of mimicry research is purely molecular rather than ecological. However, it can be considered that molecular approaches are not specific to a particular type of mimicry system, and it therefore makes more sense to deal with this topic in a single chapter and to discuss ecological approaches in the chapters that focus on each type of floral mimicry.