Role of Epigenetic Mechanisms in Host-Pathogen-Coevolution

Professor Dr. Andreas Vilcinskas

The superior goal of the priority program 1399 is to constitute host-parasite-coevolution as a model to analyze mechanisms of evolutionary adaptation. In the first funding period we established the lepidopteran Galleria mellonella and the parasitic fungus Metarhizium anisopliae as a powerful model system to determine reciprocal genetic adaptations between interacting parasite and host-derived effector molecules. At the same time, we discovered specific transgenerational immune priming in G. mellonella and increased virulence of M. anisopliae upon repeated host passages. Both phenomena emerge too rapidly to likely implicate genetic mechanisms. Alternatively, subsequent studies provide first evidence that pathogens can manipulate epigenetic regulation leading to transcriptional reprogramming in the infected insect host. Consequently, the proposed follow-up study aims for the first time to systematically explore the role of epigenetic mechanisms such as histone acetylation, DNA methylation and expression of microRNAs in transcriptional reprogramming of both the fungal parasite and the infected insect host. The recently established methods to analyze epigenetic mechanisms offer expansion of studies beyond the established host-parasite model (Galleria-Metarhizium) to include analysis of samples from model systems investigated in a number of collaborative projects (e.g. Tribolium castaneum-Bacillus thuringiensis) to address the question whether epigenetic mechanisms mediating rapid and reciprocal adaptations are frequent and evolutionarily conserved.