Despite fundamental insights in JAK-STAT contribution to health and disease, mechanistically our knowledge remains one-dimensional. JAK-STAT signaling components are known to interact with constituents of the chromatin remodelling machinery. However, the levels of signal integration and the changes to chromatin architecture driven by JAKs and STATs under different conditions are only beginning to emerge. We expect that our integrated analysis will yield at least the following results in the forthcoming years:
Hotspots of chromatin dynamics: We will compile a comprehensive catalogue of genomic regions in immune and structural cells that change their epigenomic state in response to JAK-STAT signaling during normal development and/or in disease.
JAK-STAT dependent epigenome signatures: The standardized quantification of different epigenome states will enable computational modelling of the effects of JAK-STAT signaling.
Regulatory networks encoded in chromatin: We will explore transcription factor footprints and cooperating molecular networks in dependence of JAK-STAT.
Database of JAK-STAT epigenomics: The integrated resource that we will create in this SFB will provide an important reference for the wider research community.
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