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The bloodstream form of the parasite  Trypanosoma brucei  obtains iron from its mammalian host by receptor-mediated endocytosis of host transferrin through its own unique transferrin receptor ( Tb TfR). Expression of  Tb TfR rapidly increases upon iron starvation by post-transcriptional regulation through a currently undefined mechanism that is distinct from the mammalian iron response system. We have created reporter cell lines by fusing the  Tb TfR 3’UTR or a control Aldolase 3’UTR to reporter genes encoding GFP or firefly Luciferase, and inserted the fusions into a bloodstream form cell line at a tagged ribosomal RNA locus. Fusion of the  Tb TfR 3’UTR is sufficient to significantly repress the expression of the reporter proteins under normal growth conditions. Under iron starvation conditions we observed upregulation of the mRNA and protein level of the  Tb TfR 3’UTR fusions only, with a magnitude and timing consistent with that reported for upregulation of the  Tb TfR. We conclude that the dynamic regulation of the  T .  brucei  transferrin receptor in response to iron starvation is mediated  via  its 3’UTR, and that the effect is independent of genomic location.

Dynamic regulation of the Trypanosoma brucei transferrin receptor in response to iron starvation is mediated via the 3’UTR