The bloodstream form of T. brucei acquires iron from transferrin via receptor-mediated endocytosis. However, it is unknown how procyclic forms that cannot bind transferrin acquire iron.
In this study, we show that the procyclic form of T. brucei efficiently takes up iron from ferric complexes via a reductive mechanism and that iron obtained using this mechanism is transported to and used in the mitochondria. The affinity of the transport system is comparable to that of Saccharomyces cerevisiae, with an apparent Km of 0.85 μM.