<p>What evolutionary processes and ecological patterns underlie the maintenance of asexual reproduction in natural populations? Although a vast body of literature offers theory to explain the existence of sexual and asexual reproduction, there has been little study of these forms of reproduction in the natural environment. In this dissertation I use a combination of field experiments, greenhouse studies, and genetic techniques to answer this question in the model plant system Boechera. </p><p>In Chapter 1, I review the utility of this system for studying ecological and evolutionary questions in general. Boechera offers an array of genetic and genomic tools, facilitated in part by a close evolutionary relationship with the model plant Arabidopsis thaliana, as well as undisturbed ecology and habitat that extends across much of North America. Additionally, the presence of apomixis (asexual reproduction via parthenogenetic formation of seeds) at the diploid level makes Boechera an ideal system for studying sex without the often-confounding factor of polyploidy; Boechera is one of very few plant groups in which this is possible. </p><p>In Chapter 2, I use a combination of microsatellite markers, flow cytometry, chromosome squashes, and morphological work to characterize apomixis, polyploidy, and species diversity in over 100 natural populations collected from central Idaho and western Montana. As in many other apomictic systems, I find that apomixis in Boechera is strongly linked to hybridization between species or between genetically divergent intraspecific lineages. I then explore associations between apomixis and ecological and topographical variables, as well as variables underlying differentiation between apomictic and sexual lineages. I find that ecological variables associated with apomixis are largely in congruence with the hypothesis of geographic parthenogenesis, and that geographic parthenogenesis is likely driven by the consequences of interspecific hybridization. We also find that apomixis is linked with disturbance and slope, with apomicts occurring in flatter locations than sexuals. </p><p>In Chapter 3, I use a large-scale field experiment comprising three years of data from two cohorts of sexual and asexual lineages to compare fitness between these two groups. I find that, despite herbivory levels that are much higher in apomicts than sexuals, apomictic fitness is consistently higher than sexual. Viability selection strongly favors apomicts, which results in a total fitness advantage for apomicts, despite variable fecundity selection. Selection varies in intensity between cohorts and among gardens. The results of a complementary greenhouse experiment show that the effects of herbivory differ by reproductive mode. Together, these experiments suggest that Red Queen dynamics may contribute to the coexistence of sex and asex in this group.</p><p>In Chapter 4, I use inter- and intraspecific F2 crosses to conduct a greenhouse study and a field experiment to explore the effects of hybridization and heterozygosity on fitness. I find that heterozygosity is favored in the field, with viability selection strongly favoring outcrossed over inbred lineages. However, hybridization results in lower survival, reproduction, and total fitness of interspecific F2 crosses, although hybrids that do reproduce produce more fruits than selfed parental lineages of both species, resulting in fecundity selection for hybrids. It is clear that the benefits of apomixis are due to hybridization, as hybrids are less fit overall. Evidence for both heterosis and outbreeding depression, dependent on lineage and on trait, are found in the field; these phenomena are not clearly associated with geographic distance between parental populations. Ongoing SNP genotyping will facilitate assessment of heterozygosity-fitness correlations as well as correlation of fitness and heterozygosity.</p> / Dissertation

The evolution of antibiotic resistance is shaped by interactions between genes, the chemical environment, and an antibiotic's mechanism of action. This thesis explores these interactions with experiments, theory, and analysis, seeking a mechanistic understanding of how different interactions between genes and drugs can enhance or constrain the evolution of antibiotic resistance. Chapter 1 investigates the effects of the chemical decay of an antibiotic. Tetracycline resistant and sensitive bacteria were grown competitively in the presence of tetracycline and its decay products. Antibiotic decay did not only remove selection for resistance, but long-lived decay products favored tetracycline sensitivity by inducing costly drug efflux pumps in the resistant strain. Selection against resistance by antibiotic-related compounds may contribute to the coexistence of drug-sensitive and resistant bacteria in nature. Chapter 2 investigates how genetic interactions can favor particular combinations of resistance-conferring mutations. All possible combinations of a set of trimethoprim resistance-conferring mutations in the drug's target gene were constructed and phenotyped. Incompatibilities between mutations arose in a high-order, not pairwise, manner. One mutation was found to induce this ruggedness and create a multi-peaked adaptive landscape. Chapters 1 and 2 observed that non-optimal expression of a drug resistance gene or a drug's target could compromise antibiotic resistance. Chapter 3 broadly characterizes non-optimal gene expression under antibiotic treatment, using a functional genetic screen to identify over one hundred pathways to antibiotic resistance through positive and negative changes in gene expression. Genes with the potential to confer antibiotic resistance were found to often go unused during antibiotic stress. The optimization of gene expression for drug-free growth was found to cause non-optimal expression under drug treatment, creating a situation where regulatory mutations can confer resistance by correcting errors in gene expression. Chapter 4 investigates whether it is beneficial to up-regulate the genes encoding antibiotic targets when they are inhibited. Drug target genes were quantitatively over-expressed, and drug resistance was found to not always increase, but alternatively to remain unchanged or even decrease. These diverse effects were explained by simple models that consider toxicity arising from gene over-expression, and mechanisms of drug action in which drugs induce harmful enzymatic reactions.

The major histocompatibility complex region (MHC) is a multi gene family present in all jawed vertebrates, with a fundamental role in vertebrate immunity. More than two decades of studies have resulted in the characterization of over a dozen MHC regions, and models of evolution explaining that the MHC has gradually increased in size and gene content since its origins without addressing their genomic context or the environmental selective forces. Furthermore, a compelling reconstruction of the evolutionary history of the MHC has been hampered due to phylogenetic gaps and the absence of comparative phylogenetic methods applied to comparative genomics. Here I reconstruct 320 MY of MHC evolution using 42 amniote genomes using improved gene annotations, genomic alignments and phylogenetic algorithms to reconstruct the evolution of the MHC at three levels of phylogenetic resolution. The first one describes 25 MY of evolution of the primate MHC using eight Human and four non-Human primate MHC haplotypes. Results suggests that highly dense gene segments have a strikingly conserved gene organization, and six conserved and highly rearranging segments overlap genes that are most commonly associated to disease. Phylogenomic analysis implies that the MHC has remained stable in gene content and size, with significantly increased duplication rates in the primate ancestors. The second one describes 280 MY of MHC evolution through the first characterization of reptilian MHC region, which combines mammalian, reptilian, Bird and amphibian characteristics, which favors the hypothesis of the existence of a primordial MHC in which natural killer receptors, CD1 and lectin genes co-exist. The Anolis MHC expands our understanding of the origins of the exceptionally small Bird MHC regions and provides further information about the organization and size of the ancestral amniote MHC. The third one compares 42 amniote MHC regions and map gene duplications and losses to further evaluate the mode and tempo of the evolution of the region. Comparative phylogenetic methods imply that the genomic and environmental factors affect the diversification of MHC during 320 My of evolution.

Humans show such strong sensitivity to whether resources are distributed fairly that they sacrifice personal gain to avoid distributional inequity. This inequity aversion plays an important role in guiding human social decision-making and appears to be ubiquitous across human populations. However, we currently do not understand whether or how inequity aversion evolved over the course of human evolution or how it develops in children. / Human Evolutionary Biology

At broad scales, community ecologists study how biogeographic factors like environmental dissimilarity and geographic distance influence community assembly and composition. At small scales, community ecologists study how one or several species interact to determine habitat partitioning and coexistence. In this dissertation, I present studies at both scales. Chapter One investigates community assembly across the Caribbean, Central, and South American radiations of Anolis lizards and Eleutherodactylid frogs to test whether oceanic islands are unique in their assembly processes. Such uniqueness is suggested by high levels of endemism on islands; however, comparable levels of endemism can be found in mainland communities. I modeled the rate of species turnover between mainland communities, with respect to geographic distance and environmental dissimilarity, and then used the mainland model to predict turnover among islands. Turnover among island communities was significantly higher than predicted from the mainland model, confirming the long-held but untested assumption that island assemblages accumulate biodiversity differently than their mainland counterparts. Chapter Two reviews the evidence for ecological character displacement (ECD), an evolutionary process whereby two resource competitors diverge from one another in phenotype and resource use, facilitating coexistence in a community. I find that, despite current scientific opinion, the evidence for ECD is equivocal; most cases of ECD pattern fail to rule out processes alternative to resource competition that could create the same pattern. I conclude that better evidence may come from real time tests of ECD. Chapters Three and Four describe just such a test in small island populations of Anolis carolinensis. In Chapter Three, I find that small island populations of A. carolinensis that have come into sympatry with a novel competitor, the invasive A. sagrei, shift their habitat use to become more arboreal, compared to allopatric populations. Consistent with prediction, individuals from sympatric populations have larger toepads with additional adhesive scales - a common adaptation to arboreality in Anolis. In Chapter Four, I describe a common garden experiment that finds that the observed toepad divergence is an evolved response, suggesting rates of divergence for toepad area and scale number on par with well known examples of contemporary evolution.

Epistasis describes non-additive interactions which affect gene expression and phenotype. It can happen on multiple levels, including on a genomic level with interactions between genes or even chromosomes affecting global patterns of gene expression. It can also happen within a gene itself, with epistatic interactions between amino acids affecting gene expression and resultant phenotypes. I present three studies in two organisms to study this phenomenon on a global-genomic scale, and also on a local-genic scale.

A long-standing question in evolutionary biology is whether adaptation will typically proceed through a few mutations with large selective effects or many mutations with small effects. Many studies have implicated few loci of major effect, but it has been predicted that small-effect mutations should exist and contribute to adaptation. However, such mutations have not been found in many studies, either because they do not exist or because the experimental design limited their detection. To determine the effects and types of mutations contributing to adaptation, I studied laboratory and wild populations of bacteria. I characterized the distribution of the effect sizes in laboratory populations of an aerobic bacterium, Methylobacterium extorquens, and studied the types of genetic changes associated with adaptation to a novel host in wild populations of Mycoplasma gallisepticum.

With an estimated 8,000-20,000 species, bivalves represent the second largest living class of molluscs (Bieler et al. 2013). Revived interest in molluscan phylogeny has resulted in a torrent of molecular sequence data from phylogenetic, mitogenomic, and phylogenomic studies. Despite recent progress, basal relationships of the class Bivalvia remain contentious, owing to conflicting hypotheses often between morphology and molecules.

The malaria parasite, Plasmodium falciparum, has a demonstrated history of adaptation to antimalarials and host immune pressure. This ability unraveled global eradication programs fifty years ago and seriously threatens renewed efforts today. Despite the magnitude of the global health problem, little is known about the genetic mechanisms by which the parasite evades control efforts. Population genomic methods provide a new way to identify the mutations and genes responsible for drug resistance and other clinically important traits.

Bacteria evolve during the colonization of human hosts, yet little is known about the selective pressures and evolutionary forces that shape this evolution. Illumination of these processes may inspire new therapeutic directions for combating bacterial infections and promoting healthy bacteria-host interactions. The advent of high-throughput sequencing has enabled the identification of mutations that occur within the human host, and various tools from computational and evolutionary biology can aid in creating biological understanding from these mutations. Chapter 1 describes recent progress in understanding within-patient bacterial adaption, focusing on insights made from genomic studies.