The Toxoplasma Acto-MyoA Motor Complex Is Important but Not Essential for Gliding Motility and Host Cell Invasion
The Toxoplasma Acto-MyoA Motor Complex Is Important but Not Essential for Gliding Motility and Host Cell Invasion
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DOI：
10.1371/journal.pone.0091819
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发表时间：
2014-03-14
期刊：
影响因子：
3.7
通讯作者：
Meissner, Markus
中科院分区：
文献类型：
--
作者：
Egarter, Saskia;Andenmatten, Nicole;Meissner, Markus
顶复门寄生虫被认为是通过滑动运动主动侵入宿主细胞。这种运动由寄生虫自身的肌动球蛋白系统提供动力，并依赖于肌动蛋白的调节聚合和解聚来产生滑动和宿主细胞穿透的力。最近的研究表明，弓形虫可以在缺乏几种入侵机制的核心成分，如运动蛋白肌球蛋白A（MyoA），微线蛋白MIC2和AMA1和肌动蛋白的情况下入侵宿主细胞，表明存在替代的入侵机制。在这里，MyoA，MLC1，GAP 45和ACT 1，滑翔机制的核心组件的作用，重新详细剖析。虽然这些组件的滑行运动和宿主细胞入侵的重要作用得到验证，突变体寄生虫仍然具有侵袭性，并没有显示出块的滑行运动，这表明其他机制必须到位，使寄生虫移动和入侵宿主细胞。寄生虫滑翔运动和入侵的一种新的，假设的模型，提出了基于渗透力产生的寄生虫的细胞质转化为运动。
Apicomplexan parasites are thought to actively invade the host cell by gliding motility. This movement is powered by the parasite's own actomyosin system, and depends on the regulated polymerisation and depolymerisation of actin to generate the force for gliding and host cell penetration. Recent studies demonstrated that Toxoplasma gondii can invade the host cell in the absence of several core components of the invasion machinery, such as the motor protein myosin A (MyoA), the microneme proteins MIC2 and AMA1 and actin, indicating the presence of alternative invasion mechanisms. Here the roles of MyoA, MLC1, GAP45 and Act1, core components of the gliding machinery, are re-dissected in detail. Although important roles of these components for gliding motility and host cell invasion are verified, mutant parasites remain invasive and do not show a block of gliding motility, suggesting that other mechanisms must be in place to enable the parasite to move and invade the host cell. A novel, hypothetical model for parasite gliding motility and invasion is presented based on osmotic forces generated in the cytosol of the parasite that are converted into motility.