The Role of Clathrin in Post-Golgi Trafficking in Toxoplasma gondii
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| Authors: | Manuela S Pieperhoff Miriam Schmitt David J P Ferguson Markus Meissner |
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| Institution: | 1. Wellcome Trust Centre for Molecular Parasitology, Institute of Infection, Immunity & Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.; 2. Mammalian Cell Cycle Control Mechanisms, German Cancer Research Center, Heidelberg, Germany.; 3. Nuffield Department of Clinical Laboratory Medicine, University of Oxford, Oxford, United Kingdom.; Centre National de la Recherche Scientifique, France, |
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| Abstract: | Apicomplexan parasites are single eukaryotic cells with a highly polarised secretory system that contains unique secretory organelles (micronemes and rhoptries) that are required for host cell invasion. In contrast, the role of the endosomal system is poorly understood in these parasites. With many typical endocytic factors missing, we speculated that endocytosis depends exclusively on a clathrin-mediated mechanism. Intriguingly, in Toxoplasma gondii we were only able to observe the endogenous clathrin heavy chain 1 (CHC1) at the Golgi, but not at the parasite surface. For the functional characterisation of Toxoplasma gondii CHC1 we generated parasite mutants conditionally expressing the dominant negative clathrin Hub fragment and demonstrate that CHC1 is essential for vesicle formation at the trans-Golgi network. Consequently, the functional ablation of CHC1 results in Golgi aberrations, a block in the biogenesis of the unique secretory microneme and rhoptry organelles, and of the pellicle. However, we found no morphological evidence for clathrin mediating endocytosis in these parasites and speculate that they remodelled their vesicular trafficking system to adapt to an intracellular lifestyle. |
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