Newly identified protein called BILBO1 fatal to Trypanosoma brucei

Trypanosoma brucei is a pathogen that causes epidemics of human and animal sleeping sickness in central and Southern Africa, a disease that is fatal if untreated. A new paper published this week in the open-access journal PLoS Biology investigates the formation of a trypanosome structure called the Flagellar Pocket (FP).

The work, by Derrick Robinson and colleagues at the University of Bordeaux, describes a newly identified protein called BILBO1 that is crucial for Flagellar Pocket formation; experimental inhibition of the protein BILBO1 is fatal to Trypanosoma brucei.

The Flagellar Pocket is a part of the single-celled pathogen that has several functions. As well as being the site where the flagellum attaches-the flagellum being a structure that enables the bug to propel itself-the FP is the site of endo- and exocytosis, processes that transport material in and out of the pathogen from the outside world. The FP also plays an important role in allowing the trypanosome to avoid the immune system of the host. The FP permits the trypanosomes' surface proteins (the structures seen by the immune system) to be changed, so that the bug can remain camouflaged from the host's defences. Dr. Robinson comments that "The Flagellar Pocket is a multi-tasking organelle but we can now consider it as the parasite's Achilles heel."

How the trypanosome forms this important structure has previously been unknown. The new paper, by Bonhivers et al., shows that BILBO1 is crucial for the formation of the FP; specifically, it is an important component of a part of the FP called the Flagellar Pocket Collar. BILBO1 is a cytoskeletal protein (the cytoskeleton being a network of proteins that provide internal structure for a cell), thus BILBO1 is involved in creating the cytoskeletal framework that supports the FP. This paper described the effect of preventing BILBO1 expression in the trypanosome. Without BILBO1, the trypanosome is unable to create a new FP; with the FP disrupted, it is unable to regulate endo- and exocytosis, therefore preventing it from taking up nutrients. These factors prove fatal to the trypanosome. Therefore, this work provides a target for anti-sleeping sickness drugs: knock out BILBO1 function and you will kill the trypanosome.

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