| সংক্ষিপ্ত: | The understanding that bacteria possess cooperative behaviors raises new questions as to the relevance that cooperative dynamics in bacterial populations have towards issues of human health. Significant portions of the <em>P. aeruginosa</em> genome are dedicated to producing excreted products which, by their extracellular nature, are potentially social. Given that the benefits of these excreted products are not limited to the producing cell, the potential for social cheating arises – in which selection for nonproducing cheats becomes favored – potentially jeopardizing the overall maintenance of cooperation. The degree to which extracellular processes may be considered social, and their susceptibility to cheating, will vary depending on factors such as population structure and diffusibility.
Many of these excreted products play vital roles as virulence factors during the progression of disease. Understanding the extent to which these processes exhibit social dynamics not only enhances our comprehension of pathogenesis but also opens avenues for potential treatments. Processes vulnerable to social cheating can highlight critical cellular mechanisms with high degrees of social interaction, offering opportunities for future treatments targeting specific processes or, in the case of a ‘Trojan Horse’ strategy, the cooperative behavior itself. In this thesis, I pursue three objectives: (1) Investigating iron uptake in <em>P. aeruginosa</em>, a process involving multiple mechanisms with varying degrees of cooperation. In the case of pyoverdine loss, I examine to what extent <em>P. aeruginosa</em> can compensate for the loss of this highly cooperative process. (2) I evaluate the <em>las</em>R/I quorum sensing system in P. aeruginosa as a model cooperative system for an intentional cheat-invasion strategy (3) I develop further a plant model in <em>V. radiata</em>, to identify QS factors involved with virulence and assess their potential for social cheating.
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