A MORN Repeat Protein Facilitates Protein Entry into the Flagellar Pocket of Trypanosoma brucei
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Updated: Apr 4, 2026

High-throughput Gene Tagging in Trypanosoma brucei
Published on: August 12, 2016
Brooke Morriswood1, Katy Schmidt2
1Max F. Perutz Laboratories, University of Vienna, Medical University of Vienna, Vienna, Austria brooke.morriswood@uni-wuerzburg.de katy.schmidt@meduniwien.ac.at.
Abstract:
The parasite Trypanosoma brucei lives in the bloodstream of infected mammalian hosts, fully exposed to the adaptive immune system. It relies on a very high rate of endocytosis to clear bound antibodies from its cell surface. All endo- and exocytosis occurs at a single site on its plasma membrane, an intracellular invagination termed the flagellar pocket. Coiled around the neck of the flagellar pocket is a multiprotein complex containing the repeat motif protein T. brucei MORN1 (TbMORN1). In this study, the phenotypic effects of TbMORN1 depletion in the mammalian-infective form of T. brucei were analyzed. Depletion of TbMORN1 resulted in a rapid enlargement of the flagellar pocket. Dextran, a polysaccharide marker for fluid phase endocytosis, accumulated inside the enlarged flagellar pocket. Unexpectedly, however, the proteins concanavalin A and bovine serum albumin did not do so, and concanavalin A was instead found to concentrate outside it. This suggests that TbMORN1 may have a role in facilitating the entry of proteins into the flagellar pocket.
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