Institute of Structural and Molecular Biology, Department of Biological Sciences, Birkbeck, University of London, London, United Kingdom.
School of Life Sciences, University of Nottingham, Nottingham, United Kingdom.
J Biol Chem. 2021 Nov;297(5):101063. doi: 10.1016/j.jbc.2021.101063. Epub 2021 Aug 8.
Plasmodium parasites cause malaria and are responsible annually for hundreds of thousands of deaths. Kinesins are a superfamily of microtubule-dependent ATPases that play important roles in the parasite replicative machinery, which is a potential target for antiparasite drugs. Kinesin-5, a molecular motor that cross-links microtubules, is an established antimitotic target in other disease contexts, but its mechanism in Plasmodium falciparum is unclear. Here, we characterized P. falciparum kinesin-5 (PfK5) using cryo-EM to determine the motor's nucleotide-dependent microtubule-bound structure and introduced 3D classification of individual motors into our microtubule image processing pipeline to maximize our structural insights. Despite sequence divergence in PfK5, the motor exhibits classical kinesin mechanochemistry, including ATP-induced subdomain rearrangement and cover neck bundle formation, consistent with its plus-ended directed motility. We also observed that an insertion in loop5 of the PfK5 motor domain creates a different environment in the well-characterized human kinesin-5 drug-binding site. Our data reveal the possibility for selective inhibition of PfK5 and can be used to inform future exploration of Plasmodium kinesins as antiparasite targets.
疟原虫寄生虫引起疟疾,每年导致数十万人死亡。驱动蛋白是微管依赖性 ATP 酶的超家族,在寄生虫复制机制中发挥重要作用,是抗寄生虫药物的潜在靶点。驱动蛋白-5(Kinesin-5)是一种交联微管的分子马达,在其他疾病环境中是一种既定的抗有丝分裂靶点,但在疟原虫中的机制尚不清楚。在这里,我们使用冷冻电镜对疟原虫驱动蛋白-5(PfK5)进行了表征,以确定该分子马达在核苷酸依赖性微管结合结构中的位置,并将单个马达的 3D 分类引入我们的微管图像处理管道中,以最大限度地提高我们的结构见解。尽管 PfK5 存在序列差异,但该马达表现出经典的驱动蛋白机械化学特性,包括 ATP 诱导的亚结构域重排和覆盖颈部束的形成,这与其正向定向运动一致。我们还观察到 PfK5 马达结构域中的环 5 插入创造了人源驱动蛋白-5 药物结合位点中一个不同的环境。我们的数据揭示了 PfK5 选择性抑制的可能性,并可用于指导未来对疟原虫驱动蛋白作为抗寄生虫靶点的探索。