Inorganic Phosphate Export by the Retrovirus Receptor XPR1 in Metazoans
Inorganic Phosphate Export by the Retrovirus Receptor XPR1 in Metazoans
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DOI：
10.1016/j.celrep.2013.05.035
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发表时间：
2013-06-01
期刊：
影响因子：
8.8
通讯作者：
Battini, Jean-Luc
中科院分区：
文献类型：
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作者：
Giovannini, Donatella;Touhami, Jawida;Battini, Jean-Luc
无机磷酸盐吸收是由存在于生命世界中的转运蛋白完成的普遍功能。相比之下，在后生动物中尚未发现磷酸盐输出者。在这里，我们发现，XPR1（一种最初被确定为异嗜性和多向性鼠白血病逆转录病毒（X-和P-MLV）的细胞表面受体的多通道膜分子）的耗尽会导致磷酸盐输出减少，而重新引入从果蝇到人类的各种XPR1蛋白可以挽救这种缺陷。在所有测试的人类细胞系中，以及来自肾近端小管（磷酸盐稳态调节的主要部位）的多种干细胞和上皮细胞中，使用 X-MLV 的包膜受体结合结构域产生的可溶性配体也能抑制磷酸盐输出。这些结果为后生动物磷酸盐输出以及 Xpr1 在此功能中的作用提供了新的见解。
Inorganic phosphate uptake is a universal function accomplished by transporters that are present across the living world. In contrast, no phosphate exporter has ever been identified in metazoans. Here, we show that depletion of XPR1, a multipass membrane molecule initially identified as the cell-surface receptor for xenotropic and polytropic murine leukemia retroviruses (X- and P-MLV), induced a decrease in phosphate export and that reintroduction of various XPR1 proteins, from fruit fly to human, rescued this defect. Inhibition of phosphate export was also obtained with a soluble ligand generated from the envelope-receptor-binding domain of X-MLV in all human cell lines tested, as well as in diverse stem cells and epithelial cells derived from renal proximal tubules, the main site of phosphate homeostasis regulation. These results provide new insights on phosphate export in metazoans and the role of Xpr1 in this function.