Phenotypic variation is one of the most conspicuous features of living organisms. Often this variation has a genetic origin, so individuals differ because they carry different genes. However, genetically identical individuals can still express different phenotypes depending on the environment that they encounter or even as a result of stochastic events. In this thesis I studied phenotypic variation generated by these different sources across various bacterial species. I found that there is strong phenotypic variation within clonal bacterial populations undergoing feast-and-famine cycles. This variation arises from the dynamics of resource uptake and metabolism during starvation and allows bacteria to break a fundamental life-history trade-off between growth and survival to stressors like antibiotics. I also studied how bacteria use quorum sensing to adjust their phenotype in response to external cues. Using bacterial competence as a model system, I showed how quorum-sensing signal transduction pathways can integrate information on both the abiotic and biotic environment of a cell allowing bacteria to collectively track and respond to environmental changes. Finally, I also investigated genetic diversification in the context of drug resistance evolution and found that spatial heterogeneity in the distribution of drugs inside the body can speed up the evolution of multidrug resistance during combinaton therapy. Overall, this work illustrates that a systems-level perspective spanning across different levels of biological organization is essential to understand the origin and functional relevance of phenotypic variation as well as its influence on evolutionary processes.
|Qualification||Doctor of Philosophy|
|Place of Publication||[Groningen]|
|Publication status||Published - 2020|