Martin Luther University Halle-Wittenberg

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Dipl. Biol. Sophie Helbing



Research Interests

The main intention of my PhD thesis is the determination of the gene regulatory network underlying the socially mediated immune prophylaxis. Social insect colonies are composed of closely related individuals living under high density conditions thereby providing an optimal environment for parasite establishment and transmission. To combat the infection, insects possess individual as well as group-level defenses, which are assumed to play a major role in the immune response of social insects as they might compensate for the lack of immune genes detected for honeybees and several ant species when compared to non-social species. As previous studies have shown density-dependent effects on immune-system activation in eusocial bumblebees - indicating the impact of the social context - I want to gain insights into the complex gene regulatory network underlying this socially mediated immune prophylaxis. Therefore, I want to identify the genes contributing to the social context dependent immune system activation based on a comparative transcriptomics approach by means of RNAseq utilizing isolated and group-kept bumblebees, which will be immune challenged or not. Additional experiments, pointed towards the identification of optimal group sizes and temporal duration of the main experiment, are planned. Further investigations comprise the trade-off hypothesis concerning antimicrobial activity and phenoloxidase activity as well as the effects of group sizes and density (interaction frequency) of workers.

During my diploma thesis I quantified the impact of host-parasite conflict-effects on the evolution of RNAi genes in social insects. Therefore six RNAi loci were partially amplified and compared across different species of the genus Bombus. Hence, I could show that RNAi genes exhibit an elevated rate of adaptive evolution comparing them with non-immunity genes, assuming a co-evolutionary interplay between RNAi genes and viruses, as the latter may evade hosts defense mechanisms by production of suppressor-proteins that interfere with the RNAi- pathway.