Higher eukaryotes consist of a variety of cell types and tissues. The normal development and function of these tissues requires elaborate mechanisms for individual cells to send signals and exchange information. For this purpose cells use secreted signaling molecules that bind to receptors on the surface of neighboring cells where they can activate intracellular signal transduction cascades. Mutations that disrupt the regulation of these signaling pathways often lead to abnormal tissue development or function and uncontrolled cell proliferation which are the hallmarks of cancer.
In order to develop strategies that prevent and reverse these malignant developments we must understand the mechanisms regulating the activity of signaling pathways at the molecular level. We therefore use the fruitfly Drosophila melanogaster as a model system to investigate the molecular genetic mechanisms of cell communication.
In addition to aberrant cell proliferation and differentiation, cancer is also characterized by abnormal cell behavior such as cell shape changes, cell division and cell migration. The driving force for these processes is generated by the dynamic reorganization of the actin cytoskeleton. Small GTPases of the Rho-family that are activated by GTP-exchange factors play important roles in this process. Many GTP exchange factors are oncogenes and have been isolated due to their transforming activity. We investigate the function of GTP exchange factor-dependent signaling pathways during morphogenesis of the Drosophila embryo. We are particularly interested in molecular mechanisms acting at the interface of cell fate determining signaling pathways and cytoskeletal regulators that control morphogenesis.
A genome-wide sequence analysis has shown that two thirds of all human disease genes known to date are conserved in Drosophila. The powerful Drosophila model system with its highly developed molecular genetics techniques, is therefore an excellent tool to investigate the gene networks and developmental pathways controlling invertebrate and vertebrate development as well as human disease.