As the malaria parasite, Plasmodium falciparum, grows within its host erythrocyte it induces an increase in the permeability of the erythrocyte membrane to a range of low-molecular-mass solutes, including Na+ and K+ (ref. 1). This results in a progressive increase in the concentration of Na+ in the erythrocyte cytosol. The parasite cytosol has a relatively low Na+ concentration and there is therefore a large inward Na+ gradient across the parasite plasma membrane. Here we show that the parasite exploits the Na+ electrochemical gradient to energize the uptake of inorganic phosphate (P(i)), an essential nutrient. P(i) was taken up into the intracellular parasite by a Na+-dependent transporter, with a stoichiometry of 2Na+:1P(i) and with an apparent preference for the monovalent over the divalent form of P(i). A P(i) transporter (PfPiT) belonging to the PiT family was cloned from the parasite and localized to the parasite surface. Expression of PfPiT in Xenopus oocytes resulted in Na+-dependent P(i) uptake with characteristics similar to those observed for P(i) uptake in the parasite. This study provides new insight into the significance of the malaria-parasite-induced alteration of the ionic composition of its host cell.

译文

由于疟原虫恶性疟原虫在其宿主红细胞内生长,因此引起红细胞膜对一系列低分子质量溶质 (包括Na和K) 的渗透性增加 (参考文献1)。这会导致红细胞胞质溶胶中Na的浓度逐渐增加。寄生虫胞质溶胶的Na浓度相对较低,因此在整个寄生虫质膜上存在较大的向内Na梯度。在这里,我们表明寄生虫利用Na电化学梯度来激发无机磷酸盐 (P(i)) 的吸收,这是一种必需的营养素。P(i) 被Na依赖性转运蛋白吸收到细胞内寄生虫中,化学计量为2Na: 1P(i),并且明显偏爱单价而不是P(i) 的二价形式。从寄生虫中克隆了属于PiT家族的P(i) 转运蛋白 (PfPiT),并定位在寄生虫表面。爪蟾卵母细胞中PfPiT的表达导致Na依赖性P(i) 摄取,其特征与在寄生虫中观察到的P(i) 摄取相似。这项研究为疟疾寄生虫诱导的宿主细胞离子组成改变的意义提供了新的见解。

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