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A Genetic Screen to Isolate Toxoplasma gondii Host-cell Egress Mutants
Published on: February 8, 2012
猿复合体寄生虫与宿主calpains合作,以促进它们从受感染的细胞中逃脱
Rajesh Chandramohanadas1, Paul H Davis, Daniel P Beiting
1Department of Pharmacology, University of Pennsylvania, Philadelphia, PA 19104, USA.
像Plasmodium和Toxoplasma这样的寄生原生动物使用宿主calpain蛋白酶来逃脱. 抑制calpain阻断了寄生虫的退出,而恢复它允许寄生虫退出宿主细胞.
科学领域:
- 细胞生物学 细胞生物学
- 寄生虫学的寄生虫学
- 分子生物学分子生物学
背景情况:
- 猿复合体寄生虫导致全球疾病负担显著.
- 这些原生动物在细胞内复制,必须从细胞外出才能传播.
研究的目的:
- 为了研究宿主细胞calpain蛋白酶在apicomplexan寄生虫退出中的作用.
- 为了确定calpains是否对Plasmodium falciparum和Toxoplasma gondii有必要,请退出.
主要方法:
- 使用免疫减弱,药物抑制,RNA干扰和遗传删除.
- 采用了细胞生物学和遗传补充方法.
- 研究了Plasmodium falciparum从红细胞和Toxoplasma gondii从纤维细胞的退出.
主要成果:
- 卡尔帕因-1的抑制或耗尽阻断了Plasmodium falciparum从红细胞的退出.
- 在添加纯化的calpain-1.1后,Egress被恢复.
- 托克索普拉斯马淋巴菌的退出被卡尔帕因抑制或删除所抑制.
- 在这两种寄生虫模型中,遗传补充恢复了退出.
结论:
- 宿主细胞的calpain蛋白酶对于虫复合体寄生虫的退出至关重要.
- 准幼代表了抑制寄生虫传播的潜在策略.
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