Under the Dobzhansky-Muller model, postzygotic isolation results from incompatibility between interacting genes. Evidence points to regulatory networks as a rich source of incompatibilities that impact hybrid fitness. Pleiotropy is a natural feature of regulatory networks because regulatory elements generally have multiple targets. Both pleiotropy and hybrid incompatibility arise due to genetic interactions; therefore we can expect an intimate association between them. In the following chapters, I investigate the relationship between pleiotropy and hybrid incompatibility in the context of regulatory networks. In chapter one, I extend a general network-based study of hybrid incompatibility by incorporating a sequence-based thermodynamic model of transcriptional regulation. In the absence of pleiotropy, hybrid misregulation of a positively selected trait evolves quickly as a consequence of non-recognition or spurious binding in regulatory interactions across species boundaries. In a conserved trait, hybrid incompatibility evolves much slower as a product of compensatory drift. In chapter two, I show that pleiotropy can promote or constrain the evolution of hybrid incompatibility in a regulatory network depending on its fitness landscape, which emerges from the thermodynamic properties of molecular binding. Pleiotropy may promote hybrid incompatibility in accordance with the "selection, pleiotropy, and compensation model" of evolution, in which compensation for the pleiotropic side-effects of adaptation accelerates incompatibility in conserved traits. Pleiotropy can limit the evolution of hybrid incompatibility by constraining change in trans-acting regulatory elements in favor of adaptation at less pleiotropic downstream cis-regulatory targets. Without change in both interactors, incompatibility does not occur under the Dobzhansky-Muller model. In chapter three, I evaluate the hypothesis that pleiotropy facilitates the onset of hybrid incompatibility under antagonistic coevolution, an ubiquitous and persistent source of natural selection. When infectivity and resistance in a host-parasite system are determined epistatically by network interactions, reciprocal selective pressure results in a genotypic chase. This causes pleiotropic mutations to accumulate and be compensated over time, producing intrinsic hybrid incompatibility in both species independent of local adaptation. Thus, cyclical antagonistic coevolution eventually overcomes constraint on pleiotropic loci, facilitating the evolution of regulatory incompatibilities commonly observed in hybrids.

Small bacterial genomes are believed to be evolutionarily derived from larger genomes through massive loss of genes and are usually associated with symbiotic or pathogenic lifestyles. It is therefore intriguing that a similar phenomenon of genome reduction has been reported within a group of free-living phototrophic marine cyanobacteria Prochlorococcus. Here I have investigated the roles of natural selection and mutation rate in the process of Prochlorococcus genome size reduction. Using a data set of complete cyanobacterial genomes including 12 Prochlorococcus and a sister group of 5 marine Synechococcus , I first reconstructed the steps leading to Prochlorococcus genome reduction in a phylogenetic context. The result reveals that small genome sizes within Prochlorococcus were largely determined by massive gene loss shortly after the split of Prochlorococcus and Synechococcus (a process we refer to as early genome reduction). A maximum likelihood approach was then used to estimate changes in both selection effect and mutation rate in the evolutionary history of Prochlorococcus. I also examined the effect of selection and functional importance of a subset of ancestor-derived genes those are lost in Prochlorococcus but are still retained in the genomes of its sister Synechococcus group. It appears that the effect of purifying selection was strongest when a large number of small effect genes were deleted from nearly all functional categories. And during this period, mutation rate also accelerated. Based on these results, I propose that shortly after Prochlorococcus diverged from its common ancestor with marine Synechococcus, its population size increased quickly and thus the efficacy of selection became very high. Due to limited nutrients and relatively constant environment, selection favored a streamlined genome for maximum economies in material and energy, causing subsequent reduction in genome size and possibly also contributing to the observed higher mutation rate.

<p>Population differentiation is both one of the central processes underlying the diversity that we observe in the natural world, and a mechanism that can be used to differentiate between evolutionary forces both at the level of the polymorphism, and at the level of the entire genome. Here, I use simulated evolution to analyze the statistical power to detect signals of selection in artificially selected laboratory populations, and use genomic data from wild populations of the clam shrimp Eulimnadia texana to identify genomic signals of selection in wild populations. Several loci in the wild populations appear to be under selection, and I analyze the types of genes that appear to contribute to differentiation of these populations. Additionally, I describe an analysis of genome assembly techniques that allowed for the creation of a highly contiguous genome assembly in the clam shrimp. I find that a pipeline that uses custom software to combine the results of several different genome assemblers is capable of producing genomes using long-read genomic sequencing data that are orders of magnitude more contiguous that pre-long-read methods. Simulations of experimental evolution indicated that extremely high levels of replication were necessary in order to achieve high power to detect signals of selection in experimental evolution. To this end, I describe a set of replicate experimentally evolved populations of E. texana that can be used to identify regions under selection with much higher power than could be accomplished with earlier experimental evolution schemes.

Differential psychologists rightly identified evolutionary theory as a unifying framework for explaining the origins and persistence of individual differences in a wide array of human psychological characteristics. Psychological diversity occurs on multiple levels, including between species, populations, generations, and individuals. Each level reveals the outcome of evolutionary processes at different temporal scales. I embrace a range of methods and results from quantitative and population genetics, developmental evolution, and phylogenetically grounded comparative psychology to explore how personality evolves in humans and nonhuman primates. At the level of species, I compared personality structure derived from rater assessments for four species of macaques and found a consistent, core set of personality dimensions (Dominance, Confidence, and Friendliness) describing these species. At the population level, I studied the relationship in humans between fertility/longevity trade-offs and the average personality of a country and found that Neuroticism and Agreeableness exhibit adaptively plasticity to life-history conditions. At the level of families, I estimated the quantitative genetic structure of personality in orang-utans and found that, like humans, a large portion of the phenotypic variance was explained by non-additive genetic effects. I examined between generation changes in personality by testing whether personality traits in humans are genetically correlated with fitness and found that in modern environments personality evolves very slowly. Finally, I translated current conceptual models of biological reactivity and stress response into mathematical models of developmental evolution and determined that evolution would select highly resilient phenotypes but that variation could be maintained by skew in the distribution of underlying genetic factors. From these results I broadly conclude that primate personality structure is generally conserved among species, mean personality levels change only very slowly between human generations, and that this evolution results in a genetic basis of personality that is characterized by epistasis. The evolution of individual differences has much to gain from the rigorous application of evolutionary methodology.

No description available.

Thesis (B.D.)--Western Evangelical Seminary, 1955. / Includes bibliographical references (leaves [108]-111).

Thesis (Ph. D.)--University of Michigan, 1984. / Includes bibliographical references.

Thesis (B.D.)--Western Evangelical Seminary, 1955. / Includes bibliographical references (leaves [108]-111).

<p> Unraveling the molecular etiology of a novel phenotype is still a major challenge. Mammalian pregnancy, a novel phenotype, preserves its stepwise evolution in extant species, which gives us additional tools to use to begin to unravel its evolution. Within this thesis, the evolution of three components of pregnancy are explored- the regulation of <i>TAP2</i> expression, the regulation of HLA-F expression, and the possible role of transposable elements in rewiring the regulatory networks underlying major gene expression shifts at the maternal-fetal interface.</p><p>

<p> Climate change is ostensibly one of the greatest modern selective pressures, and species with sensitive life histories or physiologies must adapt, migrate, or buffer its effects to persist. Some 15&ndash;37% of species are expected to be endangered or extinct by 2050. The most vulnerable include habitat specialists, local endemics, and species with low intrinsic growth rates. Yosemite toads (<i>Anaxyrus canorus</i>) are one such alpine endemic, having been extirpated from up to 69% of their historical range. Several features of their natural history make them vulnerable: small population sizes, high larval mortality, infrequent breeding, and specialized, patch-limited habitat prone to premature desiccation. In addition to their role as ecosystem flagships, Yosemite toads provide a model system for the many other specialists with similar life histories that are challenged by environmental change. The goal of this dissertation is to understand how historical evolutionary processes such as lineage divergence and secondary admixture, along with current levels of genetic connectivity, are expected to shape the future of Yosemite toad persistence in the face of climate change. The first chapter reconstructs phylogeographic patterns of lineage formation and fusion during repeated bouts of Pleistocene glaciation, and showcases a role for refugia in ecological divergence. The second chapter examines three contact zones as replicate tests of the hypothesis that loci associated with incipient speciation are distinct from those that readily cross ancient lineage boundaries. The third chapter models modern genetic connectivity as a network of environmental and climatic interactions, using a novel approach that incorporates phylogeographic structure. The fourth chapter forecasts the future selective pressure of climate change, and predicts where connectivity may be a mitigating force to restore genetic diversity. My dissertation provides an example of how conservation strategies can incorporate the many temporal processes (ancient, recent, and current) that have shaped current genetic diversity patterns, and use a &ldquo;total evidence&rdquo; approach to predict future adaptive potential.</p><p>