No description available.

In recent decades we have learned that cooperation is an important and pervasive feature of microbial life. This revelation raises exciting possibilities. On the one hand, we can now augment our understanding of how social phenomena evolve by using microbial model systems to test our theories. On the other hand, we can use concepts from social evolution to gain insight into the biology of the microbes we hope to control or kill. In this thesis I explore both possibilities. First, I consider the theoretical problem of how and when microbial cooperation might be subject to frequency- and densitydependence. Formerly, vague theory and a scant, sometimes contradictory empirical literature made it unclear when such patterns could be expected. Here, I develop theory tailored to a microbial context, and in each case, I test key predictions from the theory in laboratory experiments, using as my model trait the production of siderophores by the bacterium Pseudomonas aeruginosa. Secondly, I consider the ecological consequences of cooperator-cheat dynamics in the context of an infection. Specifically, I use experimental infections of diverse host models to investigate the role of two cooperative traits, siderophore production and quorum sensing, in the pathogenesis of P. aeruginosa. When a successful infection requires cooperation among pathogens, theory predicts that conflict among coinfecting strains can undermine cooperation and hence decrease virulence; whereas, in the absence of cooperation, conflict could lead to heightened exploitation and hence increased virulence. This exciting idea has received little empirical attention to date but here I address this using multiple pathogen strains, multiple social traits, and multiple model hosts.

Microbes rely on collective behaviours, such as communication and cooperation to survive and form communities. The majority of these social behaviours are mediated by the secretion of public good molecules into a shared environment such that they can be utilized by neighbouring cells. Therefore, individuals that engage in costly cooperative behaviour are susceptible to exploitation by selfish cheats that gain the benefit of cooperation without investing their share of the public good cost. Understanding such bacterial social interactions and the underlying molecular mechanisms gives insight into their complex social life in natural environments and can be used to develop alternative treatments for pathogenic bacteria that rely on such social interactions for virulence and to infect hosts. In this thesis I examine social behaviours expressed by the opportunistic pathogen, Pseudomonas aeruginosa. I develop an understanding of bacterial social dynamics, particularly competitive dynamics between cooperator and cheat strains and strains that engage in bacteriocin-mediated chemical warfare. I investigate bacterial cheat-cooperator systems in several ways: 1) I begin with a review describing the evolution of and response to cheating across a range of organisms and discuss the confusion that arises in identifying cheats particularly in microbial studies and therefore propose a key to identify cheating behaviour. 2) I empirically test whether cheating behaviour is context dependent in bacterial populations and reveal that the ability to cheat varies with the abiotic and social environment, which are two fluctuating conditions in natural environments. 3) I take an experimental approach to investigate why cheat invasion is not commonly observed in natural bacterial populations by testing the effect of cooperative bacterial growth dynamics on cheating ability. I find that secretion of public goods varies with bacterial growth dynamics and physiological growth stages which may explain why cheat invasion is more commonly observed in lab cultures and not in established natural populations. 4) In the final chapter I experimentally use natural isolates to examine the role of bacteriocins in mediating competition in pathogenic populations and find that contrary to empirical and theoretical work, bacteriocins do not play a significant role in strain competitive success and dominance. The thesis has laid groundwork for studying and understanding the role of social behaviours in bacterial systems and for further exploring social dynamics in natural bacterial populations.

Bacteria interact with one another in many ways, through helpful behaviours like producing fitness-enhancing secretions and signals as well as harmful ones like the release of anti-competitor toxins. These interactions are essential for bacterial growth and survival and can have substantial impacts on the virulence of bacterial pathogens. This thesis explores the theory of social interactions among bacteria, focusing on both the mechanisms that underlie them as well the consequences for pathogens coinfecting a host. I first propose a hypothesis for the regulation of competitive traits in bacteria. By analysing published literature on anti-competitor toxin regulation I suggest that one of the principal mediators of antagonistic behaviour in bacteria is sensing harm from competitors. In particular, I argue that certain types of stress responses, known to protect bacteria from environmental assault, are fundamental in allowing bacteria to sense competitive threats. Next I focus on another mechanism of sensing social partners, quorum sensing, which has been argued alternatively to either sense bacterial cell density or the mass transfer properties of an environment. I propose a hypothesis on how the use of multiple quorum sensing signals molecules, a common feature across many bacteria, can potentially help resolve ambiguity between social and physical aspects of a cell’s environment. The rest of the thesis focuses on the epidemiology of coinfection, bacterial and otherwise. In some parasites, high coinfection rates lead to an increased level of evolved virulence due to competition between lineages inside the host. In contrast, when cooperative secretions contribute to virulence, the opposite can occur because high producing virulent strains are out-competed by parasites that do not produce public goods. I develop a mathematical model to show that the structure of parasites inside the host largely determines the fate of virulence when there is social interaction at a local level within the host. This analysis shows that multiplicity of infection can have either a positive or negative effect on virulence depending on structuring within the host. Lastly I explore how host contact structure influences coinfection rates and show that when hosts have very heterogeneous numbers of contacts, a small fraction of individuals in the population has a disproportionate effect on coinfection, which in turn shapes pathogen evolution.

In social and biological evolution, infelicity can operate as a driving motor to force change. In this essay, for life other than human, infelicity is equated with physical unfitness to compete for the resources of a specific niche. For humanity it is defined as the result of an incongruity between a nation's culture and its government. The purpose of this study is to investigate how, for irrational life, unfitness can stimulate the creation of a new species and, for men, how the unhappiness of a nation may enhance its opportunity to enter a new socio-economic order. An evolutionary account about a possible way in which life could have evolved is offered, concentrating mainly on the transition from ape to a less remote ancestor of man, but also taking into consideration other life forms. Then, a parallel to social evolution is established. A study of the rise of capitalism in England, as well as the recent attempts to institute socialism in Latin America, are also explained as consequences of infelicity. / Graduation date: 1994

Revideret udgave af disputats 1999. / Originally presented as the author's thesis (doctoral)--Universität Hamburg, 1999.

This thesis studies the role of learning as a mechanism of economic change. Two areas are considered where this would seem to be important. First, how firms learn about new technology; and secondly, how agents learn to behave in interactive situations. A model of research and development is presented which models the process by which firms solve specific design problems. This may be by individual experimental search or by partial imitation. In the latter case, a close parallel is drawn between biological evolution, based on genetic reproduction, and technological evolution, based on firms blending existing technologies. Some economic implications of these processes are explored, including their application to stochastic learning curves, patent design and the transfer of technology to developing countries. The thesis continues by critically assessing the analogy between biological and cultural evolution often used to model how agents learn to behave in interactive situations. It is argued that the methods used by economists exploiting this analogy are often ill-suited to an economic context. Models are presented which deal with specific issues in the transition from a biological context to an economic context, including models of partnership formation, models of imperfect imitation, and models without payoff-monotonic dynamics. The issue of imperfect imitation is expanded upon in an evolutionary model of the infinitely repeated prisoners' dilemma, where it is shown that the problem of inter-generational copying fidelity may allow one to restrict attention to strategies with a very simple stochastic structure.

Thesis (M.A.)--Victoria University of Wellington, 2008. / Includes bibliographical references.

Thesis (Ph.D.) - University of St Andrews, November 2009. / Restricted until 5th November 2011.

Social projection is the tendency to project one's own characteristics onto others. This phenomenon can potentially explain cooperation in prisoner's dilemma experiments and other social dilemmas. The social projection hypothesis has recently been formalized for symmetric games as co-action equilibrium and for general games as consistent evidential equilibrium. These concepts have been proposed to predict choice behavior in experimental one-shot games. We test the predictions of the co-action equilibrium concept in a simple binary minimizer game experiment. We find no evidence of social projection.