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

• Published in: Nature communications Vol. 5; no. 1; p. 4098
• Main Authors: Lamarque, Mauld H., Roques, Magali, Kong-Hap, Marie, Tonkin, Michelle L., Rugarabamu, George, Marq, Jean-Baptiste, Penarete-Vargas, Diana M., Boulanger, Martin J., Soldati-Favre, Dominique, Lebrun, Maryse
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 17.06.2014; Nature Publishing Group
• Subjects: 14/63; 38/109; 38/70; 38/77; 631/250/255/1715; 631/80/304; Antigens, Protozoan - genetics; Antigens, Protozoan - metabolism; Gene Deletion; Genetics; Humanities and Social Sciences; Humans; Infectious diseases; Malaria; Models, Molecular; multidisciplinary; Parasites; Plasticity; Protein Binding; Protozoan Proteins - genetics; Protozoan Proteins - metabolism; Science; Science (multidisciplinary); Toxoplasma - genetics; Toxoplasma - metabolism; Toxoplasma - pathogenicity; Toxoplasmosis; Toxoplasmosis - parasitology; Vector-borne diseases; Virulence
• DOI: 10.1038/ncomms5098
• ISSN: 2041-1723

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. Apicomplexan parasites such as Toxoplasma gondii and Plasmodium form a tight, moving junction with host cells before invading them. Here the authors show that the proteins AMA1 and RON2 of T. gondii cooperate during junction formation and identify additional proteins that have a role in this process.