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    首頁> 外文期刊>Biochimica et Biophysica Acta. General Subjects >Reduced glycerol incorporation into phospholipids contributes to impaired intra-erythrocytic growth of glycerol kinase knockout Plasmodium falciparum parasites
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    Reduced glycerol incorporation into phospholipids contributes to impaired intra-erythrocytic growth of glycerol kinase knockout Plasmodium falciparum parasites

    機譯:甘油摻入磷脂的減少導致甘油激酶敲除的紅細胞內生長受損惡性瘧原蟲寄生蟲

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    摘要

    Background Malaria is a devastating disease and Plasmodium falciparum is the most lethal parasite infecting humans. Understanding the biology of this parasite is vital in identifying potential novel drug targets. During every 48-hour intra-erythrocytic asexual replication cycle, a single parasite can produce up to 32 progeny. This extensive proliferation implies that parasites require substantial amounts of lipid precursors for membrane biogenesis. Glycerol kinase is a highly conserved enzyme that functions at the interface of lipid synthesis and carbohydrate metabolism. P. falciparum glycerol kinase catalyzes the ATP-dependent phosphorylation of glycerol to glycerol-3-phosphate, a major phospholipid precursor. Methods The P. falciparum glycerol kinase gene was disrupted using double crossover homologous DNA recombination to generate a knockout parasite line. Southern hybridization and mRNA analysis were used to verify gene disruption. Parasite growth rates were monitored by flow cytometry. Radiolabelling studies were used to assess incorporation of glycerol into parasite phospholipids. Results Disruption of the P. falciparum glycerol kinase gene produced viable parasites, but their growth was significantly reduced to 56.5 ± 1.8% when compared to wild type parasites. 14C-glycerol incorporation into the major phospholipids of the parasite membrane, phosphatidylcholine and phosphatidylethanolamine, was 48.4 ± 10.8% and 53.1 ± 5.7% relative to an equivalent number of wild type parasites. Conclusions P. falciparum glycerol kinase is required for optimal intra-erythrocytic asexual parasite development. Exogenous glycerol may be used as an alternative carbon source for P. falciparum phospholipid biogenesis, despite the lack of glycerol kinase to generate glycerol-3-phosphate. General significance These studies provide new insight into glycerolipid metabolism in P. falciparum.
    機譯:背景技術瘧疾是毀滅性疾病,惡性瘧原蟲是最致命的寄生蟲感染人類。了解這種寄生蟲的生物學對于確定潛在的新型藥物靶標至關重要。在每個48小時的紅細胞內無性繁殖周期中,單個寄生蟲最多可產生32個子代。這種廣泛的增殖意味著寄生蟲需要大量的脂質前體來進行膜生物發生。甘油激酶是一種高度保守的酶,在脂質合成和碳水化合物代謝的界面上起作用。惡性瘧原蟲甘油激酶催化甘油的ATP依賴性磷酸化為主要的磷脂前體-3-磷酸甘油。方法采用雙重交叉同源DNA重組技術,破壞惡性瘧原蟲甘油激酶基因,產生基因敲除寄生蟲。 Southern雜交和mRNA分析用于驗證基因破壞。通過流式細胞儀監測寄生蟲的生長速度。放射標記研究用于評估甘油摻入寄生蟲磷脂中的情況。結果惡性瘧原蟲甘油激酶基因的破壞產生了活的寄生蟲,但與野生型寄生蟲相比,它們的生長顯著降低至56.5±1.8%。相對于同等數量的野生型寄生蟲,摻入該寄生蟲膜的主要磷脂,磷脂酰膽堿和磷脂酰乙醇胺的14 C-甘油分別為48.4±10.8%和53.1±5.7%。結論惡性瘧原蟲甘油激酶是最佳的紅細胞內無性寄生蟲發育所必需的。盡管缺乏甘油激酶來產生3-磷酸甘油,外源甘油仍可以用作惡性瘧原蟲磷脂生物發生的替代碳源。一般意義這些研究為惡性瘧原蟲的甘油脂代謝提供了新的見識。

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