Prof. Dr. Markus Engstler
Chair and Professor of Cell and Developmental Biology
fon: +49-(0)931-31-84250 (PA)
Markus Engstler is a molecular cell biologist with substantial interest in infection biology and biophysics. He graduated from Christian-Albrechts-University (Kiel) where he also received a doctorate in biochemistry. Markus spent his postdoctoral time at The Rockefeller University (New York) and the Max-Planck-Institute of Biochemistry (Martinsried). He further developed his quantitative approach to study cells as project group leader at the Free University Berlin and Ludwig-Maximilians-University Munich. Following habilitation in Genetics (LMU Munich) he was appointed Professor of Genetics at Darmstadt University of Technology. Since 2009, Markus Engstler is Professor and Chair of the Department of Cell and Developmental Biology at the Julius-Maximilians-University in Wuerzburg (you can download a more formal CV here).
Research synopsis. Markus Engstler has been using African trypanosomes as cell biology model for more than 15 years. Early biochemical work unraveled trans-sialylation, a novel mechanism of protein glycosylation, which was later shown to be critically involved in pathogenesis. Research on the control of parasite development led to new paradigms for the molecular basis of trypanosome stage differentiation. Cold-shock and chemical sensing function cooperatively in the initiation of stage transition and the routing of the major surface coat proteins is differentially regulated throughout the parasite’s life cycle. The characterization and mapping of the endocytic recycling pathways in T. brucei using quantitative fluorescence and EM methods has paved the way for trypanosomes to become a more generally accepted model system. The kinetics of plasma membrane recycling is extremely fast and the parasites harbor morphologically and functionally well-defined endosomes. A novel mechanism for the sorting of GPI-anchored proteins appears to be present (not only) in trypanosomes. This work also suggested that rapid endocytosis could be essential for trypanosome survival. The parasites continuously swim and thereby generate directional flow fields on their cell surface. These flow forces become functional when the surface coat, which is dominated by variant surface glycoproteins (VSG), is attacked by host immunoglobulins. Hydrodynamic forces drag antibody-VSG complexes towards the rear of the cell, where they are endocytosed. Thus, pure physical forces can sort proteins in the plane of the plasma membrane. Currently, Markus Engstler studies evolutionary aspects of protein sorting and cellular motility. Trypanosomes are present in the blood of amazingly diverse vertebrate species from fish to birds. Furthermore, trypanosomes parasitize plants and insects. Thus, these parasites provide unique opportunities to study the molecular and cellular basis of infection. With the advent of various high-throughput technologies a truly comparative analysis of trypanosome (bio)diversity has come within reach.
Five important publications.
Engstler, M., Reuter, G., and Schauer, R. (1993). The developmentally regulated trans-sialidase from Trypanosoma brucei sialylates the procyclic acidic repetitive protein. Molecular and Biochemical Parasitology 61: 1-13.
Engstler, M., L. Thilo, F. Weise, C. G. Grünfelder, M. Boshart and P. Overath (2004) Kinetics of endocytosis and recycling of the GPI-anchored variant surface glycoprotein in Trypanosoma brucei. Journal of Cell Science, 117:1105-1115.
Engstler, M. and M. Boshart (2004) Cold shock and regulated surface protein trafficking convey sensitization to inducers of stage differentiation in Trypanosoma brucei. Genes & Development, 18: 2798-2811.
Engstler, M., T. Pfohl, S. Herminghaus, G. Wiegertjes, M. Boshart, N. Heddergott and Overath, P. (2007) Hydrodynamic protein sorting on the cell surface of trypanosomes. Cell, 131:505-515
Heddergott N., Krüger T., Babu S.B., Wei A., Stellamanns E., Uppaluri, S., Pfohl., T., Stark, H., Engstler, M. (2012) Trypanosome Motion Represents an Adaptation to the Crowded Environment of the Vertebrate Bloodstream. PLoS Pathog 8(11): e1003023. doi:10.1371/journal.ppat.1003023