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First published online 4 March 2008
doi: 10.1242/jcs.022350
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Research Article |
1 Hygieneinstitute, Department of Parasitology, University Hospital Heidelberg, Im Neuenheimer Feld 324, D-69120 Heidelberg, Germany
2 Department of Microbiology and Molecular Medicine, University of Geneva, CMU, 1, rue Michel-Servet 1211, Geneva 4, Switzerland
* Author for correspondence (e-mail: markus.meissner{at}med.uni-heidelberg.de)
Accepted 7 January 2008
Apicomplexan parasites rely on sequential secretion of specialised secretory organelles for the invasion of the host cell. First, micronemes release their content upon contact with the host cell. Second, rhoptries are discharged, leading to the formation of a tight interaction (moving junction) with the host cell, through which the parasite invades. The functional characterisation of several micronemal proteins in Toxoplasma gondii suggests the occurrence of a stepwise process. Here, we show that the micronemal protein MIC8 of T. gondii is essential for the parasite to invade the host cell. When MIC8 is not present, a block in invasion is caused by the incapability of the parasite to form a moving junction with the host cell. We furthermore demonstrate that the cytosolic domain is crucial for the function of MIC8 and can not be functionally complemented by any other micronemal protein characterised so far, suggesting that MIC8 represents a novel, functionally distinct invasion factor in this apicomplexan parasite.
Key words: Apicomplexa, Invasion, Microneme, Rhoptry, Tet system, Toxoplasma
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