In our work we address the fundamental question how alternative splicing regulates cellular function and identity; our main model systems are the mammalian circadian clock and T cell activation. In addition to its functionality we investigate mechanisms behind signal-induced, cell type specific and circadian alternative splicing. Furthermore, comparing splicing patterns between different species led to our interest in connecting alternative splicing and evolution. We employ a variety of techniques ranging from bioinformatics to RNA-protein interaction assays, in vitro splicing, minigenes and cell culture and mouse models.
Office hours: Monday 12 - 13h.