While evolution is generally thought of as a slow process, acting at long time scales, selection can also cause rapid evolutionary changes in a population in just a few generations. This is especially true for the immune system, which is under constant selection by parasites and pathogens. In this thesis I use experimental selection to study a fast selection response in parasitoid immunity in Drosophila fruit flies. By taking selection processes into the laboratory, it becomes possible to study the action of selection in a controlled environment and to replicate the process over multiple populations that share the same genetic background. By allowing only those individuals that are able to survive parasitation to reproduce we caused replicated populations to adapt to parasitoid infection. First I analyzed the changes that selection had caused in the immune response itself. The evolved lines had a higher resistance and a higher density of insect blood cells (hemocytes), especially for specific hemocyte types. However, this was only the case in unparasitized individuals, while the larvae of selected and control lines had a similar hemocyte density after an immune reponse was induced . Secondly I analyzed the genomic changes caused by selection. I found that the effects of selection on the genome were pervasive, yet very localized. This may be a consequence of the large population size and genetically variable source population of our lines. We used these regions where selection had an effect to identify candidate genes that can increase parasitoid resistance.
|Qualification||Doctor of Philosophy|
|Place of Publication||[Groningen]|
|Publication status||Published - 2015|