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Eukaryotic Cell doi:10.1128/EC.00213-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Activation of endocytosis as an adaptation to the mammalian host by trypanosomes

The Molteno Building, Department of Pathology, Tennis Court Road, University of Cambridge, Cambridge CB2 1QP, UK, School of Biological Sciences, University of Bristol, Bristol, BS8 1UG, UK and Institute of Infection and Immunology Research, University of Edinburgh, West Mains Road, Edinburgh EH9 3JT, UK

^* To whom correspondence should be addressed. Email: mcf34{at}cam.ac.uk.

	Abstract

Immune evasion in African trypanosomes is principally mediated by antigenic variation, but rapid internalization of surface-bound immune factors may contribute to survival. Endocytosis is upregulated ten-fold in bloodstream compared to procyclic forms, and surface coat remodeling accompanies transition between these life stages. Here we examined expression of endocytosis markers in tsetse stages in vivo and monitored modulation during transition from bloodstream to procyclic forms in vitro. Among bloodstream stages non-proliferative stumpy forms have endocytic activity similar to rapidly dividing slender forms, while differentiation of stumpy to procyclic forms is accompanied by rapid down-regulation of Rab11 and clathrin, suggesting modulation of endocytic and recycling systems accompanies this differentiation event. Significantly, rapid down-regulation of endocytic markers occurs upon entering the insect midgut and expression of Rab11 and clathrin remain low throughout subsequent development, which suggests that high endocytic activity is not required for remodeling the parasite surface or survival within the fly. However, salivary gland metacyclic forms dramatically increase expression of clathrin and Rab11, indicating that emergence of mammalian infective forms is coupled to re-acquisition of a high activity endocytic/recycling system. These data suggest that high endocytosis in T. brucei is an adaptation required for viability in the mammalian host.