Abstract

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.

Highlights

  • The life cycle of Trypanosoma brucei within the tsetse is one that is complex and spectacular

  • It is premature to discount a role for in situ microtubule disassembly in either the flagellum or the cytoskeleton with the other T. brucei kinesin-13 family of proteins, but based on the current understanding of how the parasite shortens its cellular and flagellar length in the tsetse, it is unlikely that the translocation of the parasite nucleus close to the posterior end of the cell is the result of cytoskeleton disassembly

  • A PROMISING TIME? A full larder of molecular tools is available to the investigator for elucidating molecular events within cultured trypanosomes

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Summary

CELLULAR AND INFECTION MICROBIOLOGY

More than meets the eye: understanding Trypanosoma brucei morphology in the tsetse. Reviewed by: Tansy C. 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 achieve infectivity in the salivary glands. 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. We conclude that with recent breakthroughs allowing for the replication of the tsetse-infection process of T. brucei in vitro, these outstanding questions can be addressed

INTRODUCTION
Ooi and Bastin
CONCLUSION
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