Glycosylphosphatidylinositol-phospholipase C (GPI-PLC) is an enzyme that has been implicated in GPI-dependent protein trafficking and phosphoinositide metabolism in the bloodstream stage of African trypanosomes. However, despite the fact that it is associated with the cytoplasmic face of internal organellar compartments, its role in general membrane trafficking has not been investigated. Using a GPI-PLC null cell line, we determine the effect of GPI-PLC deficiency on these processes. Biosynthetic trafficking of lysosomal cargo, soluble cathepsin L and membrane bound p67, are unaffected. Likewise, secretory transport, recycling and ultimate lysosomal turnover of the GPI-anchored and transmembrane glycoproteins, transferrin receptor and invariant surface glycoprotein 65, respectively, were unaffected. A significant decrease in the endocytic uptake of transferrin was observed, confirming a prior report, but ultimate delivery to the lysosome was unimpacted. These results contribute to our understanding of the roles of this enigmatic enzyme in trypanosome cell biology.

糖基磷脂酰肌醇-磷脂酶 C (GPI-PLC) 是一种酶，它与非洲锥虫血流阶段的 GPI 依赖性蛋白质运输和磷酸肌醇代谢有关。然而，尽管它与内部细胞器隔室的细胞质面相关，但尚未研究其在一般膜运输中的作用。使用 GPI-PLC 无效细胞系，我们确定 GPI-PLC 缺陷对这些过程的影响。溶酶体货物、可溶性组织蛋白酶 L 和膜结合 p67 的生物合成运输不受影响。同样，GPI 锚定和跨膜糖蛋白、转铁蛋白受体和不变表面糖蛋白 65 的分泌转运、再循环和最终溶酶体转换不受影响。观察到转铁蛋白的内吞摄取显着减少，证实了先前的报告，但最终向溶酶体的递送未受影响。这些结果有助于我们理解这种神秘酶在锥虫细胞生物学中的作用。