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恶性疟原虫酪蛋白激酶 1 与宿主细胞蛋白运输机制成分的相互作用。

Interaction of Plasmodium falciparum casein kinase 1 with components of host cell protein trafficking machinery.

机构信息

Infection and Immunity Program and Department of Microbiology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.

Monash Proteomics & Metabolomics Facility, Department of Biochemistry and Molecular Biology, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.

出版信息

IUBMB Life. 2020 Jun;72(6):1243-1249. doi: 10.1002/iub.2294. Epub 2020 May 1.

Abstract

A pool of Plasmodium falciparum casein kinase 1 (PfCK1) has been shown to localize to the host red blood cell (RBC) membrane and be secreted to the extracellular medium during trophozoite stage of development. We attempted to identify mechanisms for secretion of PfCK1 and its appearance on the RBC membrane. We found that two host proteins with established functions in membrane trafficking in higher eukaryotes, GTPase-activating protein and Vps9 domain-containing protein 1 (GAPVD1), and Sorting nexin 22, consistently co-purify with PfCK1, suggesting that the parasite utilizes trafficking pathways previously thought to be inactive in RBCs. Furthermore, reciprocal immunoprecipitation experiments with GAPVD1 identified parasite proteins suggestive of a protein recycling pathway hitherto only described in higher eukaryotes. Thus, we have identified components of a trafficking pathway involving parasite proteins that act in concert with host proteins, and which we hypothesize mediates trafficking of PfCK1 to the RBC during infection.

摘要

已证实恶性疟原虫酪蛋白激酶 1(PfCK1)聚集于宿主红细胞(RBC)膜并在滋养体阶段分泌到细胞外基质中。我们试图确定 PfCK1 的分泌机制及其在 RBC 膜上的出现方式。我们发现两种在真核生物中具有膜运输功能的宿主蛋白,GTP 酶激活蛋白和 Vps9 结构域蛋白 1(GAPVD1)和分选连接蛋白 22,与 PfCK1 一致地共纯化,表明寄生虫利用了以前认为在 RBC 中不活跃的运输途径。此外,与 GAPVD1 的相互免疫沉淀实验鉴定出寄生虫蛋白提示了一个蛋白回收途径,迄今仅在真核生物中描述过。因此,我们已经鉴定出涉及寄生虫蛋白与宿主蛋白协同作用的运输途径的成分,我们假设该途径介导 PfCK1 在感染期间向 RBC 的运输。

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