Wolbachia are intracellular, symbiotic bacteria, known for their ability to manipulate the reproduction mechanism of their arthropod hosts, for example by inducing parthenogenesis. In this thesis,... Show moreWolbachia are intracellular, symbiotic bacteria, known for their ability to manipulate the reproduction mechanism of their arthropod hosts, for example by inducing parthenogenesis. In this thesis, I studied the causes, consequences and dynamics of a parthenogenesis-inducing (PI) Wolbachia infection in two hosts, the parasitoid wasps Tetrastichus coeruleus (Hymenoptera: Eulophidae) and Asobara japonica (Hymenoptera: Braconidae). Interestingly, both T. coeruleus and A. japonica have Wolbachia-infected parthenogenetic populations and uninfected sexual populations. The main conclusions of this thesis are as follows. First, different scenarios may occur for the spread of PI-Wolbachia infection in different host species. Wolbachia has spread via vertical transmission through populations of T. coeruleus, whereas in A. japonica Wolbachia has spread via horizontal transmission. Second, different barriers may prevent migration and gene flow between Wolbachia-infected and uninfected populations in different host species. In T. coeruleus the different populations occur in different ecological environments, whereas in A. japonica there seems to be a geographical barrier between the different populations. Third, different ages of the PI-Wolbachia infection may have different consequences for the host species. The occasional male production by Wolbachia-infected A. japonica might be explained by the relatively young age of the infection. The Wolbachia infection in T. coeruleus seems to be older. Last, a PI-Wolbachia infection can have severe consequences for the sexual functionality of infected males and females. PI-Wolbachia seems to induce cytoplasmic incompatibility in infected A. japonica males. PI-Wolbachia-infected T. coeruleus females exhibited a degradation of receptivity to matings and of spermathecal morphology. Show less
