African trypanosomes are unicellular blood parasites that cause human sleeping sickness and nagana in cattle. Key to their success has been their ability to internalize essential macromolecules from their mammalian host without exposing the machinery involved to the attention of the immune system. Uniquely, endocytosis in trypanosomes is highly polarized and occurs solely at the terminus of the exocytic arm of membrane traffic: the flagellar pocket. Although this site represents less than 5% of the surface, membrane traffic here far exceeds that of any other eukaryote. Surprisingly, the molecular quantification of the trypanosome endocytic machinery has provided direct evidence for an involvement of cell motility in surface protein traffic. It is well established that flagellar motility is essential for the parasites. However, our knowledge about the swimming behavior of trypanosomes remains rudimentary, and we have no information on trypanosome motility in the most hostile natural habitat, the mammalian vasculature. Blood flow is at least 50-times faster than trypanosome motion and the width of capillaries approaches the diameter of trypanosomes. Thus, besides being constantly attacked by the host's immune system, trypanosomes have to cope with tremendous mechanical forces. The results of Mark Engstler and his research team suggest that African trypanosomes successfully exploit hydrodynamic flow for survival in the mammalian host. The hydrodynamic forces resulting from directional motility very rapidly drag surface-bound immune complexes towards the flagellar pocket, where the highly efficient endocytosis machinery internalizes them. This novel mechanism of membrane protein sorting protects trypanosomes from complement-mediated lysis and may explain why trypanosomes have to swim at all.

Please click on the link below to see Markus Engstler's CV