疟原虫PP1磷酸酶通过调节液泡的聚集来控制无性血期出口途径的启动。

IF 5.5 1区 医学 Q1 MICROBIOLOGY
PLoS Pathogens Pub Date : 2025-01-14 eCollection Date: 2025-01-01 DOI:10.1371/journal.ppat.1012455
Marie Seveno, Manon N Loubens, Laurence Berry, Arnault Graindorge, Maryse Lebrun, Catherine Lavazec, Mauld H Lamarque
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引用次数: 0

摘要

人类疟原虫恶性疟原虫的持续血期感染依赖于其宿主红细胞的分裂子的活跃出口。在这个过程中,被感染的红细胞经历了一系列的形态学事件:周围寄生液泡的聚集,液泡膜的破坏,最后红细胞膜的破裂。这些事件由两个细胞内第二信使cGMP和钙离子(Ca2+)协调,它们分别控制它们的专用激酶PKG和CDPKs的激活,从而分泌辅助膜破裂的寄生因子。我们之前已经确定了丝氨酸-苏氨酸磷酸酶PP1是周围液泡破裂所需的基本酶。在这里,我们通过结合化学遗传学和活体显微镜研究其在出口信号通路中的精确定位和功能。在有条件的PfPP1-iKO细胞系中表达了寄生物液泡形态的荧光报告,该细胞系可以监测自然和诱导的出口动力学,以及已知出口诱导剂的拯救能力。我们的结果强调了PP1在输出级联中的双重功能。首先,我们提供了进一步的证据,证明PP1通过调节胍基环化酶α的基础活性来控制第二信使cGMP的稳态,从而调节ppg依赖的下游Ca2+信号。其次,我们证明了PP1也调节寄生物液泡的聚集,因为这一步骤在pfpp1缺失的分裂体中几乎完全被取消。引人注目的是,我们的数据表明,围捕是由出口诱导剂触发的步骤,并支持其对Ca2+的依赖,因为钙离子载体A23187绕过PfPP1-null分裂体的出口缺陷,恢复适当的出口动力学并促进围捕步骤的启动。因此,本研究将磷酸酶PP1置于cGMP-PKG信号通路的上游,并为恶性疟原虫血期出口级联的第一步roundup调控提供了新的思路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The malaria parasite PP1 phosphatase controls the initiation of the egress pathway of asexual blood-stages by regulating the rounding-up of the vacuole.

A sustained blood-stage infection of the human malaria parasite P. falciparum relies on the active exit of merozoites from their host erythrocytes. During this process, named egress, the infected red blood cell undergoes sequential morphological events: the rounding-up of the surrounding parasitophorous vacuole, the disruption of the vacuole membrane and finally the rupture of the red blood cell membrane. These events are coordinated by two intracellular second messengers, cGMP and calcium ions (Ca2+), that control the activation of their dedicated kinases, PKG and CDPKs respectively, and thus the secretion of parasitic factors that assist membranes rupture. We had previously identified the serine-threonine phosphatase PP1 as an essential enzyme required for the rupture of the surrounding vacuole. Here, we address its precise positioning and function within the egress signaling pathway by combining chemical genetics and live-microscopy. Fluorescent reporters of the parasitophorous vacuole morphology were expressed in the conditional PfPP1-iKO line which allowed to monitor the kinetics of natural and induced egress, as well as the rescue capacity of known egress inducers. Our results underscore a dual function for PP1 in the egress cascade. First, we provide further evidence that PP1 controls the homeostasis of the second messenger cGMP by modulating the basal activity of guanylyl cyclase alpha and consequently the PKG-dependent downstream Ca2+ signaling. Second, we demonstrate that PP1 also regulates the rounding-up of the parasitophorous vacuole, as this step is almost completely abolished in PfPP1-null schizonts. Strikingly, our data show that rounding-up is the step triggered by egress inducers, and support its reliance on Ca2+, as the calcium ionophore A23187 bypasses the egress defect of PfPP1-null schizonts, restores proper egress kinetics and promotes the initiation of the rounding-up step. Therefore, this study places the phosphatase PP1 upstream of the cGMP-PKG signaling pathway, and sheds new light on the regulation of rounding-up, the first step in P. falciparum blood stage egress cascade.

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来源期刊
PLoS Pathogens
PLoS Pathogens MICROBIOLOGY-PARASITOLOGY
自引率
3.00%
发文量
598
期刊介绍: Bacteria, fungi, parasites, prions and viruses cause a plethora of diseases that have important medical, agricultural, and economic consequences. Moreover, the study of microbes continues to provide novel insights into such fundamental processes as the molecular basis of cellular and organismal function.
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