Our group focuses on the analysis of a conserved mechanism of cell-to-cell communication and the identification and analysis of novel proteins important for formation and function of motile cilia.
Cell-to–cell communication plays a pivotal role in regulating growth and differentiation in multicellular organisms. One highly conserved pathway for communication between cells is the Notch signaling pathway. Notch mediates local interactions between adjacent cells in a wide variety of different tissues and organisms, which is of central importance for the regulation of developmental processes and tissue homeostasis. Using the mouse as the animal model of choice, and employing a combination of biochemical, molecular genetic, and transgenic methods, we analyze the physiological roles of Notch signaling in various tissues and organs (e.g. Cordes et al., Serth et al,. Hofmann et al., Feller et al. ,Sörensen et al), how ligands differ with respect to their biochemical/signaling properties (Geffers et al, Preuße et al), how properties of ligands and their interaction with receptors are modulated by post translational modifications (Braune et al), and which regions of ligands contribute to effective receptor activation (Schuster-Gossler et al. 2016).
Cilia are projections from cells that have a stereotyped microtubule-based structure. They can be motile or immotile and have a variety of cell-type-speciﬁc structures and physiological functions. Disruption of cilia formation or function affects important signaling pathways and leads to human diseases collectively referred to as ciliopathies. Disruption of motile cilia function in humans causes a subgroup of ciliopathies called Primary Cilia Dyskinesis (PCD). We have identified the homeobox transcription factor Noto as a critical regulator of the formation of functional motile cilia in the early embryo (Ben Abdelkhalek et al , Beckers et al, Alten et al), and have identified genes with unknown functions that are regulated downstream of Noto and encode good candidates for novel components important for motile cilia formation and/or function (Stauber et al 2017). Disruption of these genes in mice cause phenotypes resembling parts or the full spectrum of PCD in human patients (e.g. Weidemann et al 2016). Ongoing projects deal with the biochemical and functional characterization of a number of these components both in vitro and in vivo, and the further analysis of mouse models.
Our projects are supported by the German Research Council (DFG)
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