How chromatin impacts the evolution of fungal pathogens

Within the nucleus, genetic material is organized as chromatin, consisting of DNA and proteins. Both components can be modified, e.g. by methylation, which controls how tightly chromatin is packed, and thus how accessible particular DNA regions are. In many eukaryotes, tightly packed chromatin, the so-called heterochromatin, occurs at repeat-rich genomic regions and is thought to suppress gene expression and limit genetic variability of these regions. Paradoxically, many filamentous pathogens, contain large repeat-rich regions that display increased rate of genetic variability. These variable genomic regions encode many so-called effectors that mediate pathogen aggressiveness. Effector genes quickly diverge to enable pathogens to adapt to changes in the plant immune system, but also to attack novel hosts. So far, knowledge on mechanisms governing genomic variability is limited, as is the role of chromatin in this processes. We use high-throughput approaches to capture chromatin modifications (bisulfite-seq, ChIP-seq, etc.) together with assays for chromatin accessibility to study how chromatin is organized. We complement these data with analyses of genetic variability of filamentous pathogens. Together, we aim to establish links between chromatin and its modifications with genomic variability, and thus to provide fundamental insights into chromatin modifications and genome evolution.