Glycosylphosphatidylinositol (GPI)-linked molecules are surface-exposed membrane components that influence the infectivity, virulence and transmission of many eukaryotic pathogens. Procyclic (insect midgut) forms of Trypanosoma brucei do not require GPI-anchored proteins for growth in suspension culture. Deletion of TbGPI8, and inactivation of the GPI:protein transamidase complex, is tolerated by cultured procyclic forms. Using a conditional knockout, we show TbGPI8 is required for social motility (SoMo). This collective migration by cultured early procyclic forms has been linked to colonization of the tsetse fly digestive tract. The SoMo-negative phenotype was observed after a lag phase with respect to loss of TbGPI8 and correlated with an unexpectedly slow loss of procyclins, the major GPI-anchored proteins. Procyclins are not essential for SoMo, however, suggesting a requirement for at least one other GPI-anchored protein. Loss of TbGPI8 initiates the transition from early to late procyclic forms; this effect was observed in a subpopulation in suspension culture, and was more pronounced when cells were cultured on SoMo plates. Our results indicate two, potentially interlinked, scenarios that may explain the previously reported failure of TbGPI8 deletion mutants to establish a midgut infection in the tsetse fly: interference with stage-specific gene expression and absence of SoMo.

中文翻译：

---

布鲁氏锥虫作为早期前环形式的持久性和社会运动依赖于糖基磷脂酰肌醇转酰胺酶

糖基磷脂酰肌醇 (GPI) 连接的分子是表面暴露的膜成分，可影响许多真核病原体的传染性、毒力和传播。布鲁氏锥虫的前环（昆虫中肠）形式不需要 GPI 锚定蛋白在悬浮培养中生长。Tb GPI8 的缺失和 GPI：蛋白转酰胺酶复合物的失活是由培养的前环形式耐受的。使用有条件的淘汰赛，我们表明Tb GPI8 是社交运动 (SoMo) 所必需的。这种通过培养的早期顺环形式的集体迁移与采采蝇消化道的定殖有关。在Tb损失的滞后期后观察到 SoMo 阴性表型GPI8 并与主要 GPI 锚定蛋白前环素的意外缓慢损失相关。然而，前环素对 SoMo 不是必需的，这表明至少需要一种其他 GPI 锚定蛋白。Tb GPI8 的丢失启动了从早期到晚期顺环形式的转变；这种效应在悬浮培养的亚群中观察到，当细胞在 SoMo 板上培养时更为明显。我们的结果表明，两种可能相互关联的情景可以解释先前报道的Tb GPI8 缺失突变体未能在采采蝇中建立中肠感染：干扰阶段特异性基因表达和缺乏 SoMo。