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Glycosylphosphatidyl-inositols in murine malaria: Plasmodium yoelii yoelii

机译:鼠类疟疾中的糖基磷脂酰肌醇:疟原虫yoelii yoelii

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摘要

Glycosylphosphatidyl-inositols (GPIs) are vital major glycoconjugates in intraerythrocytic stages of Plasmodium. Here, we report on the biosynthesis and the characterization of GPIs synthesized by the murine malarial parasite P. yoelii yoelii YM. Parasitized erythrocytes were labeled in vivo and in vitro with either radioactive nucleotide sugar precursors, ethanolamine or glucosamine. The pathway leading to the formation of GPI precursors was found to resemble that described for P. falciparum; however, in P. yoelii, the formation of an additional hydrophilic precursor containing an acid-labile modification was detected. The data suggest that this modification is linked to the fourth mannose attached to the trimannosyl backbone in an α1-2 linkage. The modification was susceptible to hydrofluoric acid (HF), but not to nitrous acid (HNO_2). Data obtained from size-exclusion chromatography on Bio-Gel P4, and Mono Q analysis of the fragments generated by HNO_2 deamination suggest that the modification is due to the presence of an additional ethanolamine linked to the fourth mannose via a phosphodiester bond.
机译:糖基磷脂酰肌醇(GPI)是疟原虫红细胞内阶段的重要主要糖结合物。在这里,我们报告由鼠疟原虫P. yoelii yoelii YM合成的GPI的生物合成和表征。体内和体外用放射性核苷酸糖前体,乙醇胺或氨基葡萄糖标记被寄生的红细胞。发现导致GPI前体形成的途径与恶性疟原虫描述的相似。然而,在约氏疟原虫中,检测到另外的包含酸不稳定修饰的亲水性前体的形成。数据表明该修饰以α1-2键与连接至三甘露糖主链的第四甘露糖连接。该修饰对氢氟酸(HF)敏感,但对亚硝酸(HNO_2)不敏感。从Bio-Gel P4上的体积排阻色谱以及通过HNO_2脱氨基产生的片段的Mono Q分析获得的数据表明,这种修饰是由于存在通过磷酸二酯键与第四个甘露糖连接的额外乙醇胺所致。

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