Kessler Henning, Herm-Götz Angelika, Hegge Stephan, Rauch Manuel, Soldati-Favre Dominique, Frischknecht Friedrich, Meissner Markus
Hygieneinstitute, Department of Parasitology, University Hospital Heidelberg, Im Neuenheimer Feld 324, D-69120 Heidelberg, Germany.
J Cell Sci. 2008 Apr 1;121(Pt 7):947-56. doi: 10.1242/jcs.022350. Epub 2008 Mar 4.
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.
顶复门寄生虫依靠专门分泌细胞器的顺序性分泌来侵入宿主细胞。首先，微线体在与宿主细胞接触时释放其内容物。其次，棒状体排出，导致与宿主细胞形成紧密相互作用（移动连接），寄生虫通过该连接侵入。对弓形虫中几种微线体蛋白的功能表征表明存在一个逐步过程。在这里，我们表明弓形虫的微线体蛋白MIC8对于寄生虫侵入宿主细胞至关重要。当不存在MIC8时，寄生虫无法与宿主细胞形成移动连接会导致侵入受阻。我们进一步证明，胞质结构域对于MIC8的功能至关重要，并且迄今为止任何其他已表征的微线体蛋白都无法在功能上对其进行补充，这表明MIC8代表了这种顶复门寄生虫中一种新的、功能独特的侵入因子。
