Genomic evolution is a continuous process that involves the accumulation of neutral and adaptive variation within DNA sequences. Duplication, a mechanism that introduces new genetic material into a genome, is thought to be the primary source of new genes that have arisen during vertebrate evolution. This hypothesis, popularized by Susumu Ohno in 1970, has transformed the field of evolutionary biology. Consequently, many evolutionary studies have concentrated on identifying examples of gene duplication and assessing their impact on the evolution of genomes. This thesis presents the identification and analysis of three examples of gene duplication involved in shaping mammalian genomes. Through these analyses, I investigate the fate of duplicated genes and discuss the potential impact of duplication on genomic evolution. The fates depicted within these studies range from the pseudogenization of recent gene duplications to the preservation of ancient duplications for over 100 million years in multiple mammalian genomes. The consequences of these fates include neofunctionalization, subfunctionalization, and gene relocation. In additional, the analyses in this thesis demonstrate different rates and directions of evolution following gene duplication. Some duplicated genes are shown to diverge gradually over time throughout mammalian evolution, while others exhibit an accelerated evolutionary rate within a specific lineage. In other rare cases, divergence is impeded such that duplicated genes evolve in synchronization, under a process known as concerted evolution. This can lead to examples showing mosaic evolution, where both divergent and concerted evolutionary signatures are observed within a single duplicated gene. Through the analyses presented in this thesis, I illustrate some of the different evolutionary histories that result from gene duplication and examine the variety of forces that influence the evolution of duplicated genes. These studies examine the role of duplication in mammalian evolution and represent a significant contribution to the growing body of knowledge in the field of evolutionary biology.

Antimicrobials have been instrumental in the treatment of infectious disease: responsible for worldwide infection control and reductions in disease-induced morbidity, and mortality. However, in every case where new chemotherapeutic agents have been introduced, resistance to them has eventually evolved. Principally, the current strategy for dealing with this problem is to invest heavily in drug development, with the hope that new drugs become available before all existing drugs lose their efficacy. Instead of focusing on the ‘development side’ of the problem, another possible strategy is to invest in methods of slowing evolution of resistance. We use a novel application of queueing theory to demonstrate that, when comparing equivalent changes in drug development versus evolution management, the latter has a much greater effect on ensuring a continued supply of effective antimicrobial agents. Our results therefore call for a reappraisal of the current emphasis on enhancing drug development as a means of managing resistance. / Thesis (Master, Biology) -- Queen's University, 2013-07-02 15:23:55.906

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The whitefly Bemisia tabaci (Hempitera: Aleyrodidae), is one of most destructive insect pests of agriculture and horticulture worldwide. B. tabaci has an extensive host-plant range, transmits several plant viruses and is a highly invasive species. Managing B. tabaci is therefore extremely problematic and expensive, with a heavy burden placed upon insecticides. Despite a broad spectrum of insecticidal chemistry available for whitefly control, resistance is widespread and insecticide resistance management (IRM) programmes have been introduced to prolong the longevity and efficacy of these compounds. In particular, resistance is commonly associated with two morphologically indistinguishable and invasive populations, known as the B and Q biotypes. The identification of these biotypes using molecular-based diagnostics has become a key feature of IRM programmes. The development of a highthroughput real-time PCR assay which was able to discriminate between B and Q biotypes is described in Chapter 3 of this project. Two major mechanisms of resistance, target-site modification (i. e. pyrethroids and the sodium channel) and enzyme detoxification (i. e. P450-based metabolism of neonicotinoids) have been widely studied in resistant B and Q biotypes of B. tabaci. The evolutionary origins of two 'knockdown resistance' mutations associated with pyrethroid resistance are described in Chapter 4. Furthermore, the neonicotinoid, imidacloprid, is one of the most successful Insecticides registered for B. tabaci; however, reports of resistance are rapidly increasing. The molecular characterisation of imidacloprid resistance in B. tabaci, and in particular, the association of a P450-enzyme (CYP6CM1) with agespecific resistance, is reported in Chapter S. The advancement in our understanding of the molecular mechanisms underlying insecticide resistance is essential to improve management strategies Implemented against this pest.

With the advent of reasoning problems in dynamic environments, there is an increasing need for automated reasoning systems to automatically adapt to unexpected changes in representations. In particular, the automation of the evolution of their ontologies needs to be enhanced without substantially sacrificing expressivity in the underlying representation. Revision of beliefs is not enough, as adding to or removing from beliefs does not change the underlying formal language. General reasoning systems employed in such environments should also address situations in which the language for representing knowledge is not shared among the involved entities, e.g., the ontologies in a multi-ontology environment or the agents in a multi-agent environment. Our techniques involve diagnosis of faults in existing, possibly heterogeneous, ontologies and then resolution of these faults by manipulating the signature and/or the axioms. This thesis describes the design, development and evaluation of GALILEO (Guided Analysis of Logical Inconsistencies Lead to Evolution of Ontologies), a system designed to detect conflicts in highly expressive ontologies and resolve the detected conflicts by performing appropriate repair operations. The integrated mechanism that handles ontology evolution is able to distinguish between various types of conflicts, each corresponding to a unique kind of ontological fault. We apply and develop our techniques in the domain of Physics. This an excellent domain because many of its seminal advances can be seen as examples of ontology evolution, i.e. changing the way that physicists perceive the world, and case studies are well documented – unlike many other domains. Our research covers analysing a wide ranging development set of case studies and evaluating the performance of the system on a test set. Because the formal representations of most of the case studies are non-trivial and the underlying logic has a high degree of expressivity, we face some tricky technical challenges, including dealing with the potentially large number of choices in diagnosis and repair. In order to enhance the practicality and the manageability of the ontology evolution process, GALILEO incorporates the functionality of generating physically meaningful diagnoses and repairs and, as a result, narrowing the search space to a manageable size.

Human rhinoviruses (HRV) are extremely common human respiratory pathogens, most commonly associated with mild upper respiratory tract infections. The three known species of HRV (HRV-A, -B and –C) are members of the family Picornaviridae and genus Enterovirus. In contrast to the enterovirus (EV-A-D) species that commonly infect the gut, HRV are generally thought to be acid labile with replication restricted to the respiratory tract. Investigations of the clinical correlations of HRV infections detected on diagnostic screening of respiratory specimens demonstrated no specific association between HRV variant and clinical presentation. For example, similar species distributions were observed in patients admitted to the ITU and those discharged with minor illness. Unexpectedly, screening of stool specimens for HRV showed a prevalence of 10% with viral loads similar to EV infections. These findings suggested that a reappraisal of HRV tropism and disease associations may be warranted. HRV-A and -B isolates were originally classified into 100 serotypes by serological neutralisation properties. As HRV-C is difficult to isolate, no attempt had been previously made to classify the wealth of available HRV-C sequences. To facilitate definition of novel HRV types and classification of HRV-C, a system was devised to divide HRV sequences into genotypically defined types. Pairwise VP1 nucleotide p-distance analysis revealed distinct thresholds between inter- and intra- type divergence and available sequences were classified into 77 HRV-A, 29 -B and 51 -C types. This provides a standardised basis for type definition and identification, allowing consistency in studies of genetic diversity, epidemiology and evolution. It has been adopted by the ICTV Picornavirus Study Group for classification of HRV. Although the occurrence of recombination has been documented within the coding region of EV, analysis of dated HRV sequences revealed an overall lack of intra-species recombination between three coding regions of HRV-B and -C. In contrast, full HRV-A type groups appeared to have been subject to a large number of recombination events, suggesting extensive recombination during the period of its diversification into types. Putative recombination breakpoints localised to the non-structural region. Within HRV-A and HRV-B, recombination within the 5ˈUTR was infrequent. However, over 60% of analysed HRV-C strains grouped within the HRV-A clade and two recombination hotspots were identified. An additional interspecies recombination event was detected between HRV-A/C in the 2A coding region, with putative breakpoints mapping to the boundaries of the C-terminal domain of the proteinase. The studies within this thesis provide evidence for a broadened understanding of the clinical significance of HRV. In addition, the assignment of HRV sequences into genotypically defined types allowed description of the observed genetic diversity and completion of analysis which reaffirmed the sporadic nature of recombination within the coding region of HRV.

For a long time, human language has been assumed to be genetically determined and therefore the product of biological evolution. It is only within the last decade that researchers have begun to investigate more closely the domaingeneral cognitive mechanisms of cultural evolution as an alternative explanation for the origins of language. Most of this more recent work focuses on the role of imperfect cultural transmission and abstracts away from the mechanisms of communication. Specifically, models developed to study the cultural evolution of language—both theoretical and computational—often tacitly assume that linguistic signals fully specify the meaning they communicate. They imply that ignoring the fact that this is not the case in actual language use is a justified idealisation which can be made without significant consequences. In this thesis, I show that by making this idealisation, we miss out on the extensive explanatory potential of an empirically attested property of language: its pragmatic plasticity. The meaning that a signal comes to communicate in a specific context usually differs to a certain degree from its conventional meaning. This thesis (i) introduces a model of the cultural evolution of language that acknowledges and incorporates the fact that communication exhibits pragmatic plasticity and (ii) explores the explanatory potential of this fact with regard to language evolution. The thesis falls into two parts. In the first part, I develop the model conceptually. I begin by analysing the components of extant models of general cultural evolution and discuss how models of language change and linguistic evolution map onto them. Innovative use is identified as the motor of cultural evolution. I then conceptualise the cognitive mechanisms underlying innovative language use and argue that they originate in pre-linguistic forms of ostensive-inferential communication. In a next step, the identified mechanisms are employed to provide a unified account of the two main explananda of evolutionary linguistics, the emergence of symbolism and the emergence of grammar. Finally, I discuss the implications of the presented analysis for the so-called proto-language debate. In the second part of the thesis, I propose a computational implementation of the developed conceptual model. This computational implementation allows for the simulation of the cultural emergence and evolution of symbolic communication and provides a laboratory-like environment to study individual aspects of this process. I employ such computer simulations to explore the role that pragmatic plasticity plays in the development of the expressivity, signal economy and ambiguity of emerging and evolving symbolic communication systems. As its main contribution to the study of language evolution, this thesis shows that a model of linguistic cultural evolution that incorporates the notion of pragmatic plasticity has the potential to explain two crucial evolutionary puzzles, namely (i) how language can emerge from no language, and (ii) how language can come to exhibit the appearance of design for communication. The proposed usage-based model of language evolution bridges the evolutionary gap between no language and language by identifying ostensive-inferential communication as the continual aspect present in both stages, and by demonstrating that the cognitive mechanisms involved in ostensive-inferential communication are sufficient for the transition from one stage to the other.

The ability to learn multiple languages simultaneously is a fundamental human linguistic capacity. Yet there has been little attempt to explain this in evolutionary terms. Perhaps one reason for this lack of attention is the idea that monolingualism is the default, most basic state and so needs to be explained before considering bilingualism. When thinking about bilingualism in this light, a paradox appears: Intuitively, learning two languages is harder than learning one, yet bilingualism is prevalent in the world. Previous explanations for linguistic diversity involve appeals to adaptation for group resistance to freeriders. However, the first statement of the paradox is a property of individuals, while the second part is a property of populations. This thesis shows that the properties of cultural transmission mean that the link between individual learning and population-level phenomena can be complex. A simple Bayesian model shows that just because learning one language is easier than two, it doesn't mean that monolingualism will be the most prevalent property of populations. Although this appears to resolve the paradox, by building models of bilingual language evolution the complexity of the problem is revealed. A bilingual is typically defined as an individual with "native-like control of two languages" (Bloomfield, 1933, p. 56), but how do we define a native speaker? How do we measure proficiency? How do we define a language? How can we draw boundaries between languages that are changing over large timescales and spoken by populations with dynamic structures? This thesis argues that there is no psychological reality to the concept of discrete, monolithic, static `languages' - they are epiphenomena that emerge from the way individuals use low-level linguistic features. Furthermore, dynamic social structures are what drives levels of bilingualism. This leads to a concrete definition of bilingualism: The amount of linguistic optionality that is conditioned on social variables. However, integrating continuous variation and dynamic social structures into existing top-down models is difficult because many make monolingual assumptions. Subsequently, introducing bilingualism into these models makes them qualitatively more complicated. The assumptions that are valid for studying the general processes of cultural transmission may not be suitable for asking questions about bilingualism. I present a bottom-up model that is specifically designed to address the bilingual paradox. In this model, individuals have a general learning mechanism that conditions linguistic variation on semantic variables and social variables such as the identity of the speaker. If speaker identity is an important conditioning factor, then `bilingualism' emerges. The mechanism required to learn one language in this model can also learn multiple languages. This suggests that the bilingual paradox derives from focussing on the wrong kind of question. Rather than having to explain the ability to learn multiple languages simultaneously as an adaptation, we should be asking how and why humans developed a flexible language learning mechanism. This argument coincides with a move in the field of bilingualism away from asking `how are monolinguals and bilinguals different?' to `how does the distribution of variation affect the way children learn?'. In this case, while studies of language evolution look at how learning biases affect linguistic variation, studies of bilingualism look at how linguistic variation affects learning biases. I suggest that the two fields have a lot to offer each other.

Collectively, my results highlight the utility of the P matrix as a tool for studying the integration of complex traits. The extreme stability of P in T. commodus suggests that it is likely to act as a constraint on the evolution of call structure in this species. This insight, together with the link between call structure and wing morphology, illustrates the value of treating evolution as a multivariate process.

Student Number : 9701675D - MSc dissertation - School of Mathematics - Faculty of Science / The role of invariants in obtaining exact solutions of di#11;erential equations is reviewed. The examples considered are nonlinear evolution type equations like the Fisher and Fitzhugh-Nagumo equations. Finally, we look directly at an equation (formulated) governing some non-Newtonian uid in a rotating system.