Shaw M K, Tilney L G
Department of Biology, University of Pennsylvania, Philadelphia, PA 19104-6018, USA.
Proc Natl Acad Sci U S A. 1999 Aug 3;96(16):9095-9. doi: 10.1073/pnas.96.16.9095.
The invasive stages of Toxoplasma gondii, an Apicomplexan parasite, actively invade their host cells in an actin-dependent way. However, despite containing biochemically significant amounts of actin, actin filaments have never been observed in these parasites. Jasplakinolide, a membrane-permeable actin-polymerizing and filament-stabilizing drug, induced the polymerization of actin filaments at the anterior end of each tachyzoite in association with the conoid, where they formed, in many cases, a prominent membrane-enclosed apical projection reminiscent of acrosomal processes of invertebrate sperm. These jasplakinolide-induced filaments decorated with myosin subfragment 1, demonstrating unequivocally that they were indeed actin. Jasplakinolide-treated tachyzoites were unable to invade host cells, but once the drug was removed the parasites were able to enter host cells. Actin polymerization at the apical end of the parasite is consistent with the role of the apical end in host-cell invasion powered by a jackhammer-like extension and retraction of the conoid complex coupled to the secretion and rearward capping of surface proteins.
顶复门寄生虫刚地弓形虫的侵入阶段会以肌动蛋白依赖的方式主动侵入宿主细胞。然而，尽管这些寄生虫含有生化意义上大量的肌动蛋白，但从未在其中观察到肌动蛋白丝。茉莉酸内酯是一种可透过细胞膜的肌动蛋白聚合和丝稳定药物，它能诱导每个速殖子前端的肌动蛋白丝聚合，且与锥体相关，在许多情况下，它们在那里形成一个突出的、有膜包被的顶端突起，让人联想到无脊椎动物精子的顶体过程。这些由茉莉酸内酯诱导形成的丝被肌球蛋白亚片段1标记，明确表明它们确实是肌动蛋白。经茉莉酸内酯处理的速殖子无法侵入宿主细胞，但一旦去除药物，这些寄生虫就能进入宿主细胞。寄生虫顶端的肌动蛋白聚合与顶端在宿主细胞侵入中的作用相一致，这一过程由锥体复合体类似手提钻的伸展和收缩驱动，并与表面蛋白的分泌和向后封闭相关。
