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First published online 13 May 2008
doi: 10.1242/jcs.023150

Journal of Cell Science 121, 1937-1949 (2008)
Published by The Company of Biologists 2008
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Research Article

A new model for hemoglobin ingestion and transport by the human malaria parasite Plasmodium falciparum

Michelle D. Lazarus, Timothy G. Schneider and Theodore F. Taraschi*

Department of Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA

* Author for correspondence (e-mail: theodore.taraschi{at}jefferson.edu)

Accepted 19 March 2008

The current model for hemoglobin ingestion and transport by intraerythrocytic Plasmodium falciparum malaria parasites shares similarities with endocytosis. However, the model is largely hypothetical, and the mechanisms responsible for the ingestion and transport of host cell hemoglobin to the lysosome-like food vacuole (FV) of the parasite are poorly understood. Because actin dynamics play key roles in vesicle formation and transport in endocytosis, we used the actin-perturbing agents jasplakinolide and cytochalasin D to investigate the role of parasite actin in hemoglobin ingestion and transport to the FV. In addition, we tested the current hemoglobin trafficking model through extensive analysis of serial thin sections of parasitized erythrocytes (PE) by electron microscopy. We find that actin dynamics play multiple, important roles in the hemoglobin transport pathway, and that hemoglobin delivery to the FV via the cytostomes might be required for parasite survival. Evidence is provided for a new model, in which hemoglobin transport to the FV occurs by a vesicle-independent process.

Key words: Plasmodium, Actin, Cytostome, Food vacuole, Hemoglobin, Malaria


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© The Company of Biologists Ltd 2008