A vacuolar iron-transporter homologue acts as a detoxifier in Plasmodium

Ksenija Slavic, Sanjeev Krishna, Aparajita Lahree, Guillaume Bouyer, Kirsten K. Hanson, Iset Vera, Jon K. Pittman, Henry M. Staines () and Maria M. Mota ()
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Ksenija Slavic: Instituto de Medicina Molecular, Faculdade de Medicina Universidade de Lisboa
Sanjeev Krishna: Institute for Infection & Immunity, St. George’s, University of London
Aparajita Lahree: Instituto de Medicina Molecular, Faculdade de Medicina Universidade de Lisboa
Guillaume Bouyer: Institute for Infection & Immunity, St. George’s, University of London
Kirsten K. Hanson: Instituto de Medicina Molecular, Faculdade de Medicina Universidade de Lisboa
Iset Vera: Instituto de Medicina Molecular, Faculdade de Medicina Universidade de Lisboa
Jon K. Pittman: Faculty of Life Sciences, University of Manchester
Henry M. Staines: Institute for Infection & Immunity, St. George’s, University of London
Maria M. Mota: Instituto de Medicina Molecular, Faculdade de Medicina Universidade de Lisboa

Nature Communications, 2016, vol. 7, issue 1, 1-10

Abstract: Abstract Iron is an essential micronutrient but is also highly toxic. In yeast and plant cells, a key detoxifying mechanism involves iron sequestration into intracellular storage compartments, mediated by members of the vacuolar iron-transporter (VIT) family of proteins. Here we study the VIT homologue from the malaria parasites Plasmodium falciparum (PfVIT) and Plasmodium berghei (PbVIT). PfVIT-mediated iron transport in a yeast heterologous expression system is saturable (Km∼14.7 μM), and selective for Fe2+ over other divalent cations. PbVIT-deficient P. berghei lines (Pbvit−) show a reduction in parasite load in both liver and blood stages of infection in mice. Moreover, Pbvit− parasites have higher levels of labile iron in blood stages and are more sensitive to increased iron levels in liver stages, when compared with wild-type parasites. Our data are consistent with Plasmodium VITs playing a major role in iron detoxification and, thus, normal development of malaria parasites in their mammalian host.

Date: 2016
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DOI: 10.1038/ncomms10403

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