Parasites are worthy adversaries. They always seem one step ahead, but ...
... is a molecular cell biologist with substantial interest in infection biology and (bio)physics. He graduated from the Christian Albrecht University of 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 approaches to study cells as a project group leader at the Free University of Berlin and the Ludwig Maximilian University of 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 of Würzburg. Among other duties, he continues to act as a member of numerous scientific advisory boards, as well as an editor for several journals. He has served as vice-dean and dean of faculty, and is founding director of the Center for Computational and Theoretical Biology (CCTB).
since 2009 Chair and Professor of Cell and Developmental Biology, University of Würzburg
2006 - 2009 Professor of Genetics, Technical University, Darmstadt
2004 Habilitation, LMU Munich
2001-2004 Research Project Leader, LMU Munich
1998-2001 Senior Staff Scientist, Free University of Berlin
1996-1998 Postdoc, MPI Martinsried
1994-1996 Postdoc, The Rockefeller University, New York
1994-1999 DKFZ postdoctoral fellow
1994 Dr. rer. nat, University of Kiel
Tel ++49 93131 84250 (PA)
Tel ++49 93131 80060
We have been using African trypanosomes as a cell biology model for more than 20 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 harbour 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.
Antibody clearance raised the question how trypanosomes actually swim and if this phenomenon is functional in natural infection. This could only be addressed in collaboration with partners in Africa on the one hand, and physicists and mathematicians on the other hand. Trypanosomes reveal an amazingly complex motion behaviour in vitro and in the diverse and crowded environments of the host. Different trypanosome species have adapted to distinct infection niches, such as the circulation or tissue spaces. And the parasites not only swim in the mammal, but also in the insect vector, where they form giant swarms. Most recent work unraveled that trypanosomes are dynamic at various scales: the first complete structures of VSGs revealed an unprecedented molecular flexibility that accounts for different populations of VSGs on the cell surface of trypanosomes diffusing at different rates.
Schuster, S., Krüger, T., Subota, I., Thusek, S., Rotureau, B., Beilhack, A., Engstler, M. (2017) Developmental adaptations of trypanosome motility to the tsetse fly host environments unravel a multifaceted in vivo microswimmer system. eLife, in press
Bartossek T, Jones NG, Schäfer C, Cvitković M, Glogger M, Mott HR, Kuper J, Brennich M, Carrington M, Smith A-S, Fenz S, Kisker C, Engstler M. (2017) Structural basis for the shielding function of the dynamic trypanosome VSG coat. Nature Microbiology, in press
Zimmermann, H., Subota, I.; Batram, C, Kramer, S, Janzen, C, Jones, N, Engstler, M (2017) A Quorum Sensing-independent Path to Stumpy Development in Trypanosoma brucei. Plos Pathogens doi: 10.1371/journal.ppat.1006324
Glogger, M., Subota, I., Pezzarossa, A., Denecke, A.-L., Carrington, M., Fenz, S.F., Engstler, M. (2017) Facilitating trypanosome imaging, Experimental Parasitology doi: 10.1016/ j.exppara.2017.03.010.
Markert SM, Bauer V, Muenz TS, Jones NG, Helmprobst F, Britz S, Sauer M, Rössler W, Engstler M, Stigloher C. (2017) 3D subcellular localization with superresolution array tomography on ultrathin sections of various species. Methods Cell Biol. 140:21-47. doi: 10.1016/bs.mcb.2017.03.004. PMID: 28528634
Glogger, M; Stichler, S; Subota, I; Bertlein, S; Spindler, M; Tessmar, J; Groll, J; Engstler, M; Fenz, SF (2017) Live-cell super-resolution imaging of intrinsically fast moving flagellates, Journal of Physics D: Applied Physics,50,7,074004
Morriswood B, Engstler M. (2017) Let's get fISSical: fast in silico synchronization as a new tool for cell division cycle analysis. Parasitology. 2017 Feb 7:1-14. doi: 10.1017/S0031182017000038. [Epub ahead of print] PMID: 28166845
Krüger, T; Engstler, M (2016) Trypanosomes–versatile microswimmers. The European Physical Journal Special Topics,225,11-12,2157-2172
Bargul,J; Jung, J; McOdimba,F; Omogo, C O; Adung’a, Vi O; Krüger, T; Masiga, DK; Engstler, M (2016) Species-specific adaptations of trypanosome morphology and motility to the mammalian host. PLoS Pathog,12,2,e1005448
Hartel AJW, Glogger M, Jones NG, Abuillan W, Batram C, Hermann A, Fenz SF, Tanaka M, Engstler M (2016) N-glycosylation enables high lateral mobility of GPI-anchored proteins at a molecular crowding threshold. Nature Communications, 2016 Sep 19;7:12870. doi: 10.1038/ncomms12870.