Host-parasite coevolution, or the evolution of host defence and parasite counter defence is predicted to associate with high selection dynamics that are crucial for the evolution of a number of biological processes, such as fitness traits related to bothantagonists and the mechanisms generating fast genetic changes. The main objective of my PhD thesis is to enhance our understanding of host-parasite coevolution as a major selective force. Hence I addressed the complex set of the predicted evolutionary consequences that are unique to host-parasite coevolution, at both the phenotypic and molecular level, for both antagonists, and across time. I used an experimental evolution approach - under controlled laboratory conditions - using the nematode Caenorhabditis elegans as a model host, and the bacterium Bacillus thuringiensis as a model parasite. I optimized the selection protocol and multiple phenotypic measurements to compare the differences in the evolutionary outcomes between coevolution, one-sided evolution, and control conditions. After 28 host generations, I found that coevolution (i) causes reciprocal changes in both host resistance and pathogen virulence, (ii) affects their life history trade-offs, and (iii) produces patterns that are clearly different from one-sided adaptation and control conditions (Chapter I). In general the consequences of host-parasite coevolution were more pronounced in the parasite except for the patterns of temporal adaptations (Chapter I). Moreover, my results gave insights into the role of males and outcrossing in the evolution of the studied host-parasite interactions. I found an opposing interference of two selective forces that act either on the inter-species level (i.e., the high selective pressure that the antagonists exert on each other; Red Queen theory) or on the intra-species level (i.e., the differences in immunity among host genders; Bateman’s principle of immunity). Males showed higher pathogen susceptibility than hermaphrodites, thus limiting but not abolishing the potential for outcrossing and recombination for fast host adaptation (Chapter II). Finally, for the parasite, we identified genetic changes in: (i) genotype frequency, (ii) the presence or combination of cry toxins, and (iii) the presence and frequency of single nucleotide polymorphisms (SNPs). The molecular analysis was done across three time points over all replicate populations. We found that the overall parasite evolution is dominated by clonal selection followed or combined with the spread of individual mutations (Chapter III)
