Understanding eco-evolutionary dynamics in cancer tumors, species invasions, and the human microbiome is vital for numerous health and economic applications. However, spatial structure and population heterogeneity make this challenging. This dissertation tackles these challenges using a population dynamics approach, wherein systems evolve through individual growth and dispersal. The bulk of this dissertation studies expanding populations, such as growing microbial colonies, species range expansions, and cancer tumors. In this context, I first study the effect of a directional bias in dispersal: I develop a model for the stochastic growth of left-right or chirally asymmetric cells that quantitatively reproduces experimental patterns in microbial colonies. Using the model, I demonstrate that chiral dispersal provides an evolutionary advantage and affects spatial population structure in expanding populations. Second, I investigate the impact of environmental structure affecting both dispersal and growth on expanding populations. I show that cooperative population expansions in a periodic environment can be pinned to a particular location or locked to specific velocities determined by the environmental periodicity. Third, I study the problem of a phenotypically heterogeneous population, with each phenotype differing in growth and dispersal abilities. I determine the exact velocity of an expanding population where phenotypes move ballistically and explain the connection to the explosive growth transition in experimental microtubule asters. The final chapter of the dissertation examines the challenge of assembling microbial communities for performing functions such as biofuel production, nitrogen fixation, or health remediation. Due to the exponential number of possible species combinations, bioengineers resort to heuristic search strategies to find the optimal community. I identify biological properties and develop statistical measures to help bioengineers estimate their chance of success in assembling an optimal community. / 2023-02-06T00:00:00Z

This project predominantly investigated the implications of spatial heterogeneity in the ecological processes of competition and infection. Empirical analysis of spatial heterogeneity was carried out using the lepidopteran species Plodia interpunctella. Using differently viscous food media, it was possible to alter the movement rate of larvae. Soft Foods allow the movement rate of larvae to be high, so that individuals can disperse through the environment and avoid physical encounters with conspecifics. Harder foods lower the movement rate of larvae, restricting the ability of individuals to disperse away from birth sites and avoid conspecifics encounters. Increasing food viscosity and lowering movement rate therefore has the effect of making uniform distributed larval populations more aggregated and patchy. Different spatial structures changed the nature of intraspecific competition, with patchy populations characterised by individuals experiencing lower growth rates and greater mortality because of the reduced food and space available within densely packed aggregations. At the population scale, the increased competition for food individuals experience in aggregations emerges as longer generational cycles and reduced population densities. Aggregating individuals also altered the outcome of interspecific competition between Plodia and Ephestia cautella. In food media that allowed high movement rates, Plodia had a greater survival rate than Ephestia because the larger movement rate of Plodia allowed it to more effectively avoid intraspecific competition. Also the faster growth rate, and so larger size, of Plodia allowed it to dominate interspecific encounters by either predating or interfering with the feeding of Ephestia. In food that restricts movement, the resulting aggregations cause Plodia to experience more intraspecific encounters relative to interspecific, reducing its competitive advantage and levelling the survival of the two species. Spatial structure also affected the dynamics of a Plodia-granulosis virus interaction and the evolution of virus infectivity. Larval aggregation forced transmission to become limited to within host patches, making the overall prevalence of the virus low. However potentially high rates of cannibalism and multiple infections within overcrowded host aggregations caused virus-induced mortality to be high, as indicated by the low host population density when virus is presented. Also aggregated host populations cause the evolution of lower virus infectivity, where less infective virus strains maintain more susceptible hosts within the aggregation and so possess a greater transmission rate. The pattern of variation in resistance of Plodia interpunctella towards its granulosis virus was found using two forms of graphical analysis. There was a bimodal pattern of variation, with most individuals exhibiting either low or high levels of resistance. This pattern was related to a resistance mechanism that is decreasingly costly to host fitness.