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myo-Inositol uptake is essential for bulk inositol phospholipid but not glycosylphosphatidylinositol synthesis in Trypanosoma brucei.

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Publication date 2012
Author Gonzalez-Salgado Amaia, Steinmann Michael E, Greganova Eva, Rauch Monika, Mäser Pascal, Sigel Erwin, Bütikofer Peter,
Project Functional genomics of nutrient transporters in Trypanosoma brucei: From physiology to pharmacology
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Original article (peer-reviewed)

Journal The Journal of biological chemistry
Volume (Issue) 287(16)
Page(s) 13313 - 23
Title of proceedings The Journal of biological chemistry
DOI 10.1074/jbc.M112.344812


myo-Inositol is an essential precursor for the production of inositol phosphates and inositol phospholipids in all eukaryotes. Intracellular myo-inositol is generated by de novo synthesis from glucose 6-phosphate or is provided from the environment via myo-inositol symporters. We show that in Trypanosoma brucei, the causative pathogen of human African sleeping sickness and nagana in domestic animals, myo-inositol is taken up via a specific proton-coupled electrogenic symport and that this transport is essential for parasite survival in culture. Down-regulation of the myo-inositol transporter using RNA interference inhibited uptake of myo-inositol and blocked the synthesis of the myo-inositol-containing phospholipids, phosphatidylinositol and inositol phosphorylceramide; in contrast, it had no effect on glycosylphosphatidylinositol production. This together with the unexpected localization of the myo-inositol transporter in both the plasma membrane and the Golgi demonstrate that metabolism of endogenous and exogenous myo-inositol in T. brucei is strictly segregated.