Abstract
Cilia and flagella perform diverse roles in motility and sensory perception, and defects in their construction or their function are responsible for human genetic diseases termed ciliopathies. Cilia and flagella construction relies on intraflagellar transport (IFT), the bi-directional movement of ‘trains’ composed of protein complexes found between axoneme microtubules and the flagellum membrane. Although extensive information about IFT components and their mode of action were discovered in the green algae Chlamydomonas reinhardtii, other model organisms have revealed further insights about IFT. This is the case of Trypanosoma brucei, a flagellated protist responsible for sleeping sickness that is turning out to be an emerging model for studying IFT. In this article, we review different aspects of IFT, based on studies of Chlamydomonas and Trypanosoma. Data available from both models are examined to ask challenging questions about IFT such as the initiation of flagellum construction, the setting-up of IFT and the mode of formation of IFT trains, and their remodeling at the tip as well as their recycling at the base. Another outstanding question is the individual role played by the multiple IFT proteins. The use of different models, bringing their specific biological and experimental advantages, will be invaluable in order to obtain a global understanding of IFT.
Highlights
Cilia and flagella perform diverse roles in motility and sensory perception, and defects in their construction or their function are responsible for human genetic diseases termed ciliopathies
When inhibition of a given gene blocked flagellum formation, it was described as an anterograde phenotype (A) and when it stopped retrograde transport, resulting in the formation of shorter flagella filled with intraflagellar transport (IFT) material, it was described as a retrograde phenotype (R)
In Trypanosoma, analysis of the traces left by Green fluorescent protein (GFP)::IFT52 from live cells suggests that the trains are at least 400 nm in length on the anterograde transport direction and 250 nm in the retrograde direction
Summary
Proteins have been grouped according to their category. When inhibition of a given gene blocked flagellum formation, it was described as an anterograde phenotype (A) and when it stopped retrograde transport, resulting in the formation of shorter flagella filled with IFT material, it was described as a retrograde phenotype (R). In Trypanosoma, analysis of the traces left by GFP::IFT52 from live cells suggests that the trains are at least 400 nm in length on the anterograde transport direction and 250 nm in the retrograde direction. These must be considered as approximations due to the limited resolution of light microscopy and the relatively long exposure time [75]. If trains contain the same amount of material on a shorter surface, the signal intensity for the GFP IFT fusion proteins should look brighter This is the opposite that is observed for all IFT proteins or motors studied so far in both Chlamydomonas and Trypanosoma [69,75,77]. The results could be explained by an equilibrated exchange between the cytoplasmic pool and the pool at the flagellum base that would be sensitive to temperature or to flagellum length
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