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

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.

Flagellar incorporation of proteins follows at least two different routes in trypanosomes

“…Again, no recovery was observed. These results demonstrate that both the heavy and the intermediate dynein chains undergo little or no turn over at the distal tip of the flagellum, supporting the view that, once assembled, mature trypanosome flagella do not modify their length [Ooi and Bastin, ].…”

“…Finally, the absence of turnover of both the heavy and the intermediate dynein chains supports the view that the length of the mature flagellum in trypanosomes is fixed [Ooi and Bastin, ]. This finding explains that absence or arrest of IFT in mature flagella had no effect on their length, contrarily to the growing flagellum [Fort et al., ].…”

Intraflagellar transport is required for the maintenance of the trypanosome flagellum composition but not length

“…This absence of shortening could be due to the sophisticated architecture of the trypanosome flagellum that contains a PFR physically connected to the axoneme and that is attached along most of the length of the cell body via another cytoskeletal structure called the flagellum attachment zone (Sunter and Gull, 2016). Accordingly, when trypanosomes produce developmental stages with a shorter flagellum length, this is always achieved by mean of an asymmetric division with the construction of a shorter new flagellum and not by shortening an existing flagellum (Ooi and Bastin, 2013;Rotureau et al, 2011;Sharma et al, 2008).…”

Transcriptome Profiling of Trypanosoma brucei Development in the Tsetse Fly Vector Glossina morsitans

“…Successful completion of the life cycle, i.e. survival in and adaptation to new surroundings, requires activation of specific and complex developmental programs which culminate in the manifestation of at least 10 distinct morphological forms [3–5]. In the mammalian bloodstream, a pleomorphic strain exists as both a long slender form that can replicate by asexual division and a cell cycle arrested short stumpy form pre-programmed to encounter the insect host [6].…”