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J. Biol. Chem., Vol. 281, Issue 42, 31995-32003, October 20, 2006

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A Conserved Region in the EBL Proteins Is Implicated in Microneme Targeting of the Malaria Parasite Plasmodium falciparum^*

Moritz Treeck, Nicole S. Struck, Silvia Haase, Christine Langer, Susann Herrmann, Julie Healer, Alan F. Cowman¹, and Tim W. Gilberger, Recipient of an Emmy-Noether fellowship (DFG)²

From the Bernhard Nocht Institute for Tropical Medicine, Malaria II, 20359 Hamburg, Germany and the The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3050, Australia

The proliferation of the malaria parasite Plasmodium falciparum within the human host is dependent upon invasion of erythrocytes. This process is accomplished by the merozoite, a highly specialized form of the parasite. Secretory organelles including micronemes and rhoptries play a pivotal role in the invasion process by storing and releasing parasite proteins. The mechanism of protein sorting to these compartments is unclear. Using a transgenic approach we show that trafficking of the most abundant micronemal proteins (members of the EBL-family: EBA-175, EBA-140/BAEBL, and EBA-181/JSEBL) is independent of their cytoplasmic and transmembrane domains, respectively. To identify the minimal sequence requirements for microneme trafficking, we generated parasites expressing EBA-GFP chimeric proteins and analyzed their distribution within the infected erythrocyte. This revealed that: (i) a conserved cysteine-rich region in the ectodomain is necessary for protein trafficking to the micronemes and (ii) correct sorting is dependent on accurate timing of expression.

Received for publication, July 14, 2006 , and in revised form, August 23, 2006.

This article is based in part on doctoral studies by M. T., N. S. S., and S. H. in the Faculty of Biology, University of Hamburg.

^* This study was supported in part by Grants from the Deutsche Forschungs-gemeinschaft (DFG, GI312), Fritz Prosiegel Stiftung and Australian Education International (AEI). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Fig. S1.

¹ Supported by HHMI International Research Scholar Grants.

² To whom correspondence should be addressed: Research Group Malaria II, Bernhard-Nocht-Institute for Tropical Medicine, Bernhard-Nocht-Strasse 74, 20359 Hamburg, Germany. Tel.: 49-0-40-42818-486; Fax: 49-0-40-42818-418; E-mail: gilberger{at}bni-hamburg.de.

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