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PTEX组件HSP101调解了各种疟疾因子向宿主红细胞的输出

Josh R Beck¹, Vasant Muralidharan², Anna Oksman³

¹1] Department of Molecular Microbiology, Washington University School of Medicine, St Louis, Missouri 63110, USA [2].

|July 22, 2014

概括

疟疾寄生虫Plasmodium falciparum使用热冲击蛋白101 (HSP101) 来在PVM中输出蛋白质. 这一依赖HSP101的步骤对于寄生虫的生存和毒性至关重要.

科学领域:

疟疾研究疟疾研究
寄生虫学的寄生虫学
分子生物学分子生物学

背景情况:

杆菌 (Plasmodium falciparum) 出口许多蛋白质,以求生存和毒性.
通过寄生虫孔真空膜 (PVM) 进行蛋白质转移的机制尚未完全理解.
导出蛋白质 (PTEX) 复合物的Plasmodium转基因被假设为介导蛋白质出口.

研究的目的:

调查热冲击蛋白101 (HSP101) 在整个PVM的蛋白质出口中的作用.
为PTEX复合体在蛋白质转位中的作用提供直接的功能证据.

主要方法:

采用了陪伴者自抑制策略,以快速,可逆地切除HSP101功能.
在出口阻塞条件下,观察到真空中蛋白质的积累.
评估了HSP101与其他PTEX组件之间的关联.

主要成果:

废除 HSP101 功能导致整个 PVM 的蛋白质出口几乎完全受阻.
这一封锁影响了所有类型的出口蛋白质,表明出口步骤趋同.
在出口封锁条件下,HSP101和PTEX组件之间的关联损失发生.

结论:

在Plasmodium falciparum的PVM中,HSP101对于蛋白质出口至关重要和普遍要求.
在寄生虫的蛋白质出口途径中,HSP101依赖转位是一个关键的,融合的步骤.
为了高效的蛋白质出口,PTEX复合物的完整性是必要的.

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