Caenorhabditis elegans and its Microparasite Bacillus thuringiensis: Consequences of Experimental Evolution for Host-Parasite-Parasite Interactions

The reciprocal evolutionary effects pathogens and their hosts have on each other are one of the most powerful selective forces in evolution, leading to adaptive phenotypic and genetic changes of both antagonists. In nature, bacterial infections often consist of more than one genotype. Since the host represents a limited resource, an interaction between the co-infecting genotypes is likely and potentially has fundamental effects on the interaction with the host. Nevertheless, most studies focus only on the interaction of parasite and host, ignoring within-host dynamics between co-infecting parasite genotypes. In my thesis, I focussed on both, the consequences of long-term host-parasite evolution for the interaction with a host and for parasite-parasite interactions. The first chapter is a comprehensive theoretical overview presenting the effects of multiple infections on virulence towards the host. It summarizes not only potential social interactions between the different co-infecting genotypes, but also discusses the relevance of their relatedness and resulting consequences for virulence. In the second chapter I present the results from a long-term evolution experiment using Caenorhabditis elegans as a multicellular host, singly infected with one of two different strains of its microparasite Bacillus thuringiensis. I found that both, coevolution with and adaptation to the host, led to rapid diversification of the clonal parasite populations into distinct clones. These clones showed strain specific phenotypic changes (i.e., killing rate and production of antagonistic substances) not only within, but also between replicate populations. In the third chapter one of these evolved clones was compared to its ancestral, non-evolved clone on the molecular level. By using next generation genome sequencing, I analysed the underlying genetic mechanisms that led to diversification within the clonal population presented in chapter two. In this study I demonstrated the importance of bacterial genomic plasticity for adaptation: the results revealed that changes were mainly caused by mobile genetic elements (MGEs), especially transposases and plasmids. Overall this thesis shows that the evolutionary selection pressure mediated by a multicellular host causes phenotypic diversification of the parasite. This change within and between parasite populations is reflected on both, the phenotypic and the genetic level