Open AccessThe moving junction of apicomplexan parasites: a key structure for invasion
Author(s) -
Besteiro Sébastien,
Dubremetz JeanFrançois,
Lebrun Maryse
Publication year - 2011
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2011.01597.x
Subject(s) - microneme , biology , rhoptry , microbiology and biotechnology , apicomplexa , gliding motility , internalization , secretion , obligate parasite , plasmodium (life cycle) , motility , parasite hosting , intracellular parasite , obligate , intracellular , host (biology) , receptor , plasmodium falciparum , immunology , malaria , genetics , ecology , biochemistry , world wide web , computer science
Summary Most Apicomplexa are obligate intracellular parasites and many are important pathogens of human and domestic animals. For a successful cell invasion, they rely on their own motility and on a firm anchorage to their host cell, depending on the secretion of proteins and the establishment of a structure called the moving junction (MJ). The MJ moves from the apical to the posterior end of the parasite, leading to the internalization of the parasite into a parasitophorous vacuole. Based on recent data obtained in Plasmodium and Toxoplasma , an emerging model emphasizes a cooperative role of secreted parasitic proteins in building the MJ and driving this crucial invasive process. More precisely, the parasite exports the microneme protein AMA1 to its own surface and the rhoptry neck RON2 protein as a receptor inserted into the host cell together with other RON partners. Ongoing and future research will certainly help refining the model by characterizing the molecular organization within the MJ and its interactions with both host and parasite cytoskeleton for anchoring of the complex.