The Interplay Between Constraint and Selection in Phenotypic Evolution

This dissertation seeks to elucidate how individual variation in ecologically important traits influences the dynamics of multi-species communities, with particular emphasis on the feedback between population dynamics and evolutionary change. I use mathematical models to investigate a range of problems under this broad theme, focusing on questions important in both basic and applied evolutionary ecology.;A central focus of my dissertation involved investigating the evolution of life history traits. I analyze the evolutionary dynamics of such traits in populations subject to anthropogenic perturbations and in natural populations not subject to such perturbations. I began by focusing on the evolutionary sustainability of alternative management regimes for the lacustrine brook char (Salvelinus fontinalis) fisheries in southern Canada. Size-selective mortality caused by fishing can impose strong selection on harvested fish populations and ultimately affect evolution in important life-history traits. Using an individual-based quantitative genetic modeling framework, I show that harvesting between 5-15% of the brook charr biomass both maximizes high yields but also mitigates harvest-induced adaptive change.;Secondly, I analyze the mechanisms by which suites of correlated life history traits (life history syndromes) evolve in unharvested, size-structured populations. Using an individual based model, I investigate how the interplay between selective factors and phylogenetic and energetic constraints influences the evolution of life history syndromes. I demonstrate how the interplay between selection driven by size-specific mortality and constraints on somatic growth drive the evolution of entire suites of life history traits towards different syndromes.;The second major focus of this dissertation concerns the ecology and evolution of host-pathogen systems. First, I modified an epidemiological model for vector-borne diseases to explore the effect of indirect ecological interactions on disease dynamics. This work shows that highly efficient predators and parasitoids of the vector prove to be effective biological control agents, but highly virulent pathogens of the vector require a high transmission rate to be effective. Moreover, I show that inundating a host-vector-disease system with a natural enemy of the vector has little or no effect on reducing disease incidence, but inundating the system with a competitor of the vector has a large effect on reducing disease incidence.;Finally, I developed an evolutionary epidemiological model to investigate the evolutionary stability of tumor specificity of genetically engineered or artificially selected oncolytic (tumor-killing) viruses. Because oncolytic viruses deplete the supply of tumor cells upon which they depend for proliferation, cancer cell tropism can be rendered maladaptive if viral treatment is highly successful. I asked under what conditions mutant viruses that attack healthy cells can evolve. I found that when the number of infectious particles released upon lysing (transmission) is constrained by the ability of viruses to lyse healthy cells (virulence), mutant strains that can exploit healthy cells are unlikely to evolve even when mutation rates are high. A trade-off between virulence and transmission imposes a high fitness cost on viral strains that can exploit healthy cells efficiently, thereby preventing evolution towards healthy cell tropism.