Thesis (M.S.)--State University of New York at Binghamton, Biological Sciences Department, 2005. / Includes bibliographical references.

Thesis (Ph. D.)--University of Texas at Austin, 2007. / Vita. Includes bibliographical references.

Thesis (M.Phil.)--Hong Kong University of Science and Technology, 2007. / Includes bibliographical references (leaves 79-82). Also available in electronic version.

'Culture' is defined as information, such as knowledge, beliefs, skills, attitudes or values, that is passed from individual to individual via social (or cultural) transmission and expressed in behaviour or artifacts. 'Cultural evolution' holds that this cultural inheritance system is governed by the same Darwinian processes as gene-based biological evolution. In Part A of this thesis it is argued that as compelling a case can now be made for a Darwinian theory of cultural evolution as Darwin himself presented in The Origin Of Species for biological evolution, If culture does indeed evolve, then it follows that the structure of a science of cultural evolution should broadly resemble that of the science of biological evolution. Hence Part A concludes by outlining a unified science of cultural evolution based on the sub-disciplines of evolutionary biology. Parts B and C comprise original empirical and theoretical work constituting two branches of this science of cultural evolution. Part B describes a series of experiments testing for a number of hypothesised biases in cultural transmission. Evidence was found for a 'social bias' that acts to promote information concerning third-party social relationships over equivalent non-social information, and a 'hierarchical bias' that acts to transform knowledge of everyday events from low-level actions into higher-level goals. Three other hypothesised biases concerning status, anthropomorphism and neoteny were not supported, although each gave rise to potential, future work using this methodology. Part C presents a theoretical investigation into the coevolution of the genetic bases of human mating behaviour and culturally inherited folk beliefs regarding paternity. Gene-culture coevolution and agent-based models suggested that beliefs in 'partible paternity' (that more than one man can father a child) create a new more polygamous form of society compared with beliefs in singular paternity (that only one man can father a child).

Orientador: Renato Eugênio da Silva Diniz / Banca: Fernanda Franzolin / Banca: Ana Maria de Andrade Caldeira / Resumo: Atualmente, o entendimento da Evolução Biológica como conceito mais importante e unificador de todos os campos da Biologia é unânime entre a comunidade científica, uma vez que todas as questões relativas às Ciências Biológicas só podem ser respondidas de maneira plena através da consideração dos aspectos evolutivos. A apreensão dos elementos e processos que integram o conceito da Evolução Biológica é considerada de fundamental importância não apenas em um âmbito educacional, mas também para o desenvolvimento intelectual e social do indivíduo. Assim sendo, esta dissertação se propôs a investigar a maneira com que o conceito da Evolução Biológica vem sendo oferecido à população do Estado de São Paulo no contexto da educação pública de nível médio, não apenas de modo a verificar sua exatidão em relação ao conhecimento científico atual, mas também considerando as aproximações e distanciamentos através dos quais seus conhecimentos são transpostos. Para tanto, foi realizada uma investigação de caráter qualitativo e documental acerca do conteúdo evolutivo encontrado no material didático oferecido à Rede Pública de Ensino do Estado de São Paulo. Os resultados encontrados evidenciam que além da precisão científica dos conhecimentos oferecidos ao nível da educação formal, é fundamental a presença de um olhar meticuloso sobre a forma com que os conceitos são apresentados, em busca não apenas de uma articulação eficiente entre os conceitos relativos à processos e mecanism... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: Currently, the understanding of Biological Evolution as the most important and unifying concept in all fields of Biology is unanimous among the scientific community, since all questions related to Biological Sciences can only be fully answered through consideration of evolutionary aspects. The apprehension of the elements and processes that integrate the concept of the Biological Evolution is considered of fundamental importance not only in an educational scope, but also for the intellectual and social development of the individual. Thus, this dissertation proposed to investigate the way in which the concept of Biological Evolution has been offered to the population of the State of São Paulo in the context of public secondary education, not only in order to verify its accuracy in relation to the current scientific knowledge, but also considering the rigor and laxity through which their knowledge is transposed. For that, a qualitative and documentary research was carried out on the evolutionary content found in the didactic material offered to the Public Education Network of the State of São Paulo. The results show that in addition to the scientific accuracy of the knowledge offered at the formal education level, it is fundamental to have a meticulous look at the way in which the concepts are presented, seeking not only an efficient articulation between the concepts related to evolutionary processes and mechanisms, but also a broad historical context related to the development... (Complete abstract click electronic access below) / Mestre

The continuing rise of antibiotic resistance is threatening a return to the world of pre-antibiotic medicine. Multi-drug resistant pathogens are already claiming lives and causing economic losses in developing and developed countries alike. We need, therefore, to understand what allows resistant strains to spread; what makes them evolutionarily competitive in and amongst other strains and species. The majority of laboratory studies of antibiotic resistance focus on simple growth in liquid culture. By contrast, microbes commonly grow as surface-associated communities, in which interactions between neighbouring cells have strong consequences for competition and evolution. My first goal was to understand how growth in such environments affects the success of a resistant strain. By competing an antibiotic resistant and susceptible strain of the pathogenic bacterium Pseudomonas aeruginosa, I found that growth in dense colonies on agar allowed a resistant strain to protect susceptible strains, to the extent that the susceptible strain may even prevail under antibiotic treatment. This effect was specific to a cooperative mechanism of antibiotic resistance, however; a β-lactamase enzyme that digests the antibiotics surrounding a resistant cell. A further, unexpected reason that susceptible cells could prevail was that they elongate under antibiotic treatment, allowing them to push shorter resistant cells aside in the competition for the growing edge of a colony. My work suggests that the rise of cooperative resistance mechanisms should be more easily suppressed than for non-social mechanisms. However, one major strategy to overcome antibiotic resistance is the use of antibiotic-adjuvants, drugs which inhibit a mechanism of antibiotic resistance. It is not clear if these adjuvants will tend to suppress or promote cooperative resistance mechanisms. I performed experiments to test the effects of inhibitory adjuvants on cooperative resistance. These revealed that the effects of adjuvants are varied. In liquid culture, an adjuvant inhibited resistance evolution, while, in colony experiments, it promoted resistance evolution by removing the cross protection of susceptible strains. Given the complexity and importance of antibiotic adjuvants, I developed an eco-evolutionary model to dissect these complexities associated with the combination of interacting microbial and molecular species. As in my experiments, the models identified conditions where an inhibitory adjuvant can increase selection for resistance. However, the theory also identifies scenarios for which adjuvants will delay resistance evolution by shutting down the associated evolutionary pathway. Broadening the modelling framework to include the stochastic effects of rare mutation, I found that early administration of adjuvant inhibitors can be a powerful way to suppress the emergence of antibiotic resistance. Microbial interactions are complex and affected by the growth environment. My thesis underlines that the study of antibiotic resistance will benefit from greater consideration of how bacteria interact and, more broadly, how their ecology and evolution determine the rise, or fall, of resistance.

ABSTRACT This dissertation describes and critiques the Darwinian proposal for morality constructed by Professor Michael Ruse. Chapter 1 outlines Ruse's background and Darwinian worldview while also depicting some inherent obstacles to the Darwinian worldview. Chapter 2 describes the moral anti-realism of Professor Ruse and illustrates his position as Hume updated by Darwin. Ruse's ethical skepticism denies genuine objectivity in morality, but he also rejects traditional subjectivism. Ruse describes himself as a subjectivist of a distinct kind. Chapter 3 examines the central and most controversial tenet of Ruse's moral proposal: the illusion of objectivity. Analysis and critique is offered of Ruse's proposal that objectivity is an illusion foisted upon all humans by natural selection. Chapter 4 describes how Ruse defines altruism and illustrates the fundamental problem that genuine altruism is for Darwinism. A charge is offered that Darwinism only supports pseudo-altruism and cannot successfully justify the common practice of authentic altruism. Chapter 5 concludes the dissertation and offers an argument that the nature of God serves as a far superior foundation for morality than Ruse supplies in his proposal. The doctrine of the imago dei provides a robust account of human dignity and morality.

Polygenic adaptation in response to selection on quantitative traits is thought to be ubiquitous in humans and other species, yet this mode of adaptation remains poorly understood. We investigate the dynamics of this process, assuming that a sudden change in environment shifts the optimal value of a highly polygenic quantitative trait. We find that when the shift is not too large relative to the genetic variance in the trait and this variance arises from segregating loci with small to moderate effect sizes (defined in terms of the selection acting on them before the shift), the mean phenotype's approach to the new optimum is well approximated by a rapid exponential process first described by Lande (1976). In contrast, when the shift is larger or large effect loci contribute substantially to genetic variance, the initially rapid approach is succeeded by a much slower one. In either case, the underlying changes to allele frequencies exhibit different behaviors short and long-term. Over the short term, strong directional selection on the trait introduces small differences between the frequencies of minor alleles whose effects are aligned with the shift in optimum versus those with effects in the opposite direction. The phenotypic effects of these differences are dominated by contributions from alleles with moderate and large effects, and cumulatively, these effects push the mean phenotype close to the new optimum. Over the longer term, weak directional selection on the trait can amplify the expected frequency differences between opposite alleles; however, since the mean phenotype is close to the new optimum, alleles are mainly affected by stabilizing selection on the trait. Consequently, the frequency differences between opposite alleles translate into small differences in their probabilities of fixation, and the short-term phenotypic contributions of large effect alleles are largely supplanted by contributions of fixed, moderate ones.

Meiotic recombination is a fundamental genetic process in all sexually reproducing eukaryotes, ultimately responsible for the generation of new combinations of alleles upon which natural selection can act. It begins with the formation of programmed double stranded breaks along the genome, and ends with their repair as non-crossover or crossover recombination events. The localization of such events along the genome has important evolutionary consequences for genome structure, base composition, patterns of genetic diversity, linkage disequilibrium and introgression, along the genome, as well as in the evolution of post-zygotic hybrid sterility and speciation. Understanding how meiotic recombination events are localized is thus crucial to the proper interpretation of observed genetic variation, and to the field of population genetics as a whole. However, little is known about how most species localize recombination events. While some species localize meiotic recombination events fairly evenly along the genome (e.g., Caenorhabditis elegans or Drosophila), most species studied to date, including all yeasts, plants and vertebrates, localize the vast majority of meiotic recombination events to narrow intervals of the genome known as recombination hotspots. Within such species, there appear to be at least two general mechanisms underlying the localization of hotspots. First, in many species, including baker’s yeast, canids, birds, and plants, the vast majority of hotspots are found in close proximity with promoter-like features of the genome, such as transcriptional start sites and CpG-islands. Recombination landscapes in these species tend to be highly conserved between closely related species. Second, in mice, primates and cattle, the vast majority of hotspots are found away from promoter-like features of the genome, and at sites bound by the PRDM9 protein, which has a rapidly evolving DNA-binding specificity. Concordantly, the recombination landscapes in these species tends to be rapidly evolving. The aim of Chapter 2 of this dissertation is to characterize the distribution of mechanisms across vertebrates indirectly, by leveraging what is known about their genetic and molecular underpinnings. In particular, I consider what is known about the molecular mechanisms and evolutionary consequences of using PRDM9 to localize recombination events, and attempt to infer which vertebrate species are or are not likely to be using PRDM9 in an analogous manner. I find that PRDM9 has been lost repeatedly within vertebrates, and, moreover, that many species carry partial PRDM9 orthologs lacking one or more feature believed to be important for its role in recombination. In Chapter 3, I demonstrate that swordtail fish, which have such a partial PRDM9 ortholog, do not use PRDM9 to localize recombination events. Instead, they use promoter-like features of the genome, similar to species lacking PRDM9 altogether. This work suggests that only species carrying complete PRDM9 orthologs are likely to use them to localize recombination events, and that upon the partial or complete loss of PRDM9, species typically default to the use of promoter-like features. Beyond more immediately practical insight, understanding the phylogenetic distribution of mechanisms by which meiotic recombination events are localized along the genome will shed light on why different species employ different mechanisms. The repeated losses of PRDM9-directed recombination across vertebrates suggests that selective pressures are not always strong enough to justify the evolutionary maintenance of PRDM9. Notably, theory suggests that PRDM9’s DNA-binding specificity has to be continually evolving in order for it to localize recombination events to hotspots. This is a consequence of gene conversion acting to remove PRDM9 binding sites from the population over time. Models have been proposed in which selection favors younger PRDM9 alleles because their binding sites have experienced less erosion due to gene conversion. Nonetheless, it has remained unclear how the loss of PRDM9 binding sites might cause a reduction in fitness, principally because it has remained unclear what the evolutionary benefit of having hotspots is more generally. Recently, however, a number of studies investigating the role of PRDM9 in mediating hybrid sterility in certain crosses of musculus subspecies have implicated the erosion of its binding sites in this process. In particular, the lineage specific erosion of PRDM9 binding sites causes, in the F1 generation, the PRDM9 alleles from each parental lineage to bind primarily to the non-parental genetic background, where its binding sites have not yet been eroded. These studies suggest that there is a benefit to the symmetric binding of PRDM9 across homologous chromosomes, and that fitness is reduced as a consequence of asymmetry in PRDM9 binding. In Chapter 4 of this dissertation I develop a population genetics based model of the co-evolution of PRDM9 and its binding sites taking into consideration these recent findings. In particular, I model competition between PRDM9 binding sites and define fitness as a function of PRDM9 binding symmetry. This model demonstrates that PRDM9 binding symmetry will decrease over time in randomly mating populations, and that selection for symmetric binding is sufficient to drive the rapid turnover of PRDM9 alleles. Importantly, the requirement for symmetry in this model shapes the recombination landscape by favoring highly skewed binding distributions. This model thus provides theoretical support for the hypothesis that a requirement for symmetry might underlie the evolutionary advantage of recombination hotspots.

The evolutionary relationships of woodrats (Neotoma) were elulcidated through phylogenetic analyses of mitochondrial DNA restriction site and allozyme data. DNA samples from eleven nominal species from the genus Neotoma and two outgroup taxa, Ototylomys phyttotis and Xenomys nelsoni, were cleaved using a suite of 17 Type II restriction endonucleases. Mitochondrial DNA restriction profiles were visualized following electrophoresis of restriction digests via methods of Southern transfer and hybridization with 32P- and digoxigenin-labeled mtDNA probes. Restriction mapping resulted in the identification of 37 unique mtDNA haplotypes among the woodrat taxa examined. Proteins representing 24 presumptive structural gene loci were examined through starch gel electrophoresis. Binary-coded allozyme data and allozyme frequency data were analyzed using PAUP and FREQPARS, respectively. Phylogenetic analyses of the mtDNA restriction site data incorporated three different character type assumptions: unordered binary characters, Dollo characters, and differentially weighted unordered characters employing the STEPMATRIX option of PAUP. Proposed phylogenies for Neotoma are based on majority-rule consensus trees produced using bootstrap procedures. Phylogenetic analyses of the woodrat data sets revealed a distinct dichotomy among populations of white-throated woodrats (N. albigula) suggesting the presence of cryptic species within that taxon. MtDNA and allozyme data support the specific status of N. devia as distinct from N. lepida, and additionally reveal the presence of a third cryptic species referable to N. intermedia among the desert woodrats. Phylogenetic analyses of the genetic data also suggest subgeneric status for the desert woodrats, which is in agreement with evidence from morphology. The genetic data revealed a sister group relationship between N. stephensi and samples of N. mexicana, suggesting the placement of N. stephensi into the N. mexicana species-group. Neotoma fuscipes and N. cinerea formed a monophyletic lineage basal to the remaining members of the subgenus Neotoma which supports the assignment of N. fuscipes to the subgenus Teonoma with N. cinerea. Although stringent, Dollo parsimony methods produced the best supported phylogenies among the species of Neotoma. The STEPMATRIX approach was unable to resolve species relationships within species-groups but clearly delineated the higher taxonomic levels between species-groups and subgenera.