You are here: Home / Research / Research Areas / Research Areas / RA II

RA II Somatic and Epigenetic Determination of Cellular Destiny


Tissue-specific effects of disease mutations, discontinuous patterns of interface affection, the chronicity of inflammatory changes and the interaction of the multiple cell types in the barrier tissue context all point to epigenetic and somatic alterations as a key factor to achieve an integrated understanding of the disease process. RA II will provide a scientific framework to address the crucial questions in this context such as: (1) How does germline disposition lead to disease manifestation? (2) Do disease genes perturb the epigenetic information at the interface? (3) What explains the cellular heterogeneity of inflammatory disease and how does this relate to the phenotype? (4) How are clinical subphenotypes and therapy response reflected on the epigenetic level? The main approach of the RA will be directed at a toponomics of inflammation, i.e. the localization of biological processes, cellular machines, chromosomes and genes inside of individual cells/organs with sufficient spatial and temporal resolution. To this end, this RA will focuse on an in-situ agenda for studying somatic changes directly in tissue samples. Moreover, the RA will drive projects investigating nuclear topology and the generation of iPSC for reprogramming primary barrier cells, and will aim at a delineation of somatic genetic/epigenetic marks in-situ in defined cellular populations.

Contribution to the Scientific Discourse

The RA will resolve somatic genetic and epigenetic changes of barrier inflammation in selected cellular populations down to the single cell level (topology of inflammation). We hypothesize that field effects and individual genomic/epigenomic compositions of cellular subpopulations critically modulate the onset and perpetuation of inflammatory diseases. The joined studies will contribute to the (1) understanding of the interplay of (somatic) genetic variation and epigenetic modifications in different cell types, (2) investigate the effects of inflammation on cellular differentiation programs (ex situ and iPSC models) and (3) describe the effects of “epigenetic” drugs on inflammatory processes.

Document Actions