Gliding motility and cell invasion are essential for the successful transmission of Plasmodium parasites. These processes rely on an acto-myosin motor located underneath the parasite plasma membrane. The Myosin A-tail interacting protein (MTIP) connects the class XIV myosin A (MyoA) to the gliding-associated proteins and is essential for assembly of the motor at the inner membrane complex. Here, we assessed the subcellular localization of MTIP in Plasmodium berghei motile stages from wild-type parasites and mutants that lack MyoA or the small heat shock protein 20 (HSP20). We demonstrate that MTIP is recruited to the apical end of motile ookinetes independently of the presence of MyoA. We also show that infective sporozoites displayed a polarized MTIP distribution during gliding, and that this distribution was abrogated in mutant parasites with an aberrant locomotion.

滑翔运动和细胞入侵对于疟原虫寄生虫的成功传播至关重要。这些过程依赖于位于寄生虫质膜下面的肌动球蛋白马达。肌球蛋白A-尾相互作用蛋白（MTIP）将XIV类肌球蛋白A（MyoA）连接到与滑行相关的蛋白，并且对于在内膜复合物处组装运动至关重要。在这里，我们评估了伯氏疟原虫中MTIP的亚细胞定位缺乏MyoA或小的热休克蛋白20（HSP20）的野生型寄生虫和突变体的活动阶段。我们证明，MTIP被独立于MyoA的存在而募集到运动的动植物的顶端。我们还显示，感染性子孢子在滑翔过程中显示出极化的MTIP分布，并且这种分布在运动异常的突变寄生虫中被废除。