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Front. Cell. Infect. Microbiol., 13 November 2013 | http://dx.doi.org/10.3389/fcimb.2013.00071

More than meets the eye: understanding Trypanosoma brucei morphology in the tsetse

  • Trypanosome Cell Biology Unit, CNRS URA2581, Institut Pasteur, Paris, France

T. brucei, the causative parasite for African trypanosomiasis, faces an interesting dilemma in its life cycle. It has to successfully complete its infection cycle in the tsetse vector to be able to infect other vertebrate hosts. T. brucei has to undergo multiple morphological changes as it invades the alimentary canal of the tsetse to finally achieve infectivity in the salivary glands. In this review, we attempt to elucidate how these morphological changes are possible for a parasite that has evolved a highly robust cell structure to survive the chemically and physically diverse environments it finds itself in. To achieve this, we juxtaposed the experimental evidence that has been collected from T. brucei forms that are cultured in vitro with the observations that have been carried out on tsetse-infective forms in vivo. Although the accumulated knowledge on T. brucei biology is by no means trivial, several outstanding questions remain for how the parasite mechanistically changes its morphology as it traverses the tsetse and how those changes are triggered. However, we conclude that with recent breakthroughs allowing for the replication of the tsetse-infection process of T. brucei in vitro, these outstanding questions can finally be addressed.

Keywords: trypanosome, tsetse, life cycle, cytoskeleton, morphological changes, stage-specific regulation

Citation: Ooi CP and Bastin P (2013) More than meets the eye: understanding Trypanosoma brucei morphology in the tsetse. Front. Cell. Infect. Microbiol. 3:71. doi: 10.3389/fcimb.2013.00071

Received: 31 July 2013; Accepted: 14 October 2013;
Published online: 13 November 2013.

Edited by:

Brice Rotureau, Institut Pasteur, France

Reviewed by:

Tansy C. Hammarton, University of Glasgow, UK
Michael Ginger, Lancaster University, UK
Eva Gluenz, University of Oxford, UK

Copyright © 2013 Ooi and Bastin. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Philippe Bastin, Trypanosome Cell Biology Unit, CNRS URA2581, Institut Pasteur, 25 Rue du Docteur Roux, Paris 75015, France e-mail: pbastin@pasteur.fr