Plasticity and redundancy among AMA–RON pairs ensure host cell entry of Toxoplasma parasites

Mauld H. Lamarque, Magali Roques, Marie Kong-Hap, Michelle L. Tonkin, George Rugarabamu, Jean-Baptiste Marq, Diana M. Penarete-Vargas, Martin J. Boulanger, Dominique Soldati-Favre and Maryse Lebrun ()
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Mauld H. Lamarque: UMR 5235 CNRS, Université de Montpellier 2
Magali Roques: UMR 5235 CNRS, Université de Montpellier 2
Marie Kong-Hap: UMR 5235 CNRS, Université de Montpellier 2
Michelle L. Tonkin: University of Victoria
George Rugarabamu: CMU, University of Geneva
Jean-Baptiste Marq: CMU, University of Geneva
Diana M. Penarete-Vargas: UMR 5235 CNRS, Université de Montpellier 2
Martin J. Boulanger: University of Victoria
Dominique Soldati-Favre: CMU, University of Geneva
Maryse Lebrun: UMR 5235 CNRS, Université de Montpellier 2

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: Abstract Malaria and toxoplasmosis are infectious diseases caused by the apicomplexan parasites Plasmodium and Toxoplasma gondii, respectively. These parasites have developed an invasion mechanism involving the formation of a moving junction (MJ) that anchors the parasite to the host cell and forms a ring through which the parasite penetrates. The composition and the assembly of the MJ, and in particular the presence of protein AMA1 and its interaction with protein RON2 at the MJ, have been the subject of intense controversy. Here, using reverse genetics, we show that AMA1, a vaccine candidate, interacts with RON2 to maintain the MJ structural integrity in T. gondii and is subsequently required for parasite internalization. Moreover, we show that disruption of the AMA1 gene results in upregulation of AMA1 and RON2 homologues that cooperate to support residual invasion. Our study highlights a considerable complexity and molecular plasticity in the architecture of the MJ.

Date: 2014
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DOI: 10.1038/ncomms5098

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