F-actin and Myosin F control apicoplast elongation dynamics which drive apicoplast-centrosome association in Toxoplasma gondii.
F-actin and Myosin F control apicoplast elongation dynamics which drive apicoplast-centrosome association in Toxoplasma gondii.
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F-肌动蛋白和肌球蛋白 F 控制弓形虫中顶质体伸长动力学，从而驱动顶质体-中心体关联。
DOI：
10.1101/2023.01.01.521342
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发表时间：
2023
期刊：
影响因子：
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通讯作者：
Heaslip,AoifeT
中科院分区：
文献类型：
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作者：
Devarakonda,ParvathiMadhavi;Sarmiento,Valeria;Heaslip,AoifeT
弓形虫含有一个重要的质体细胞器，称为顶质体，是合成脂肪酸、类异戊二烯和血红素所必需的。影响顶质体功能或遗传的扰动导致寄生虫死亡。顶质体是一个单拷贝的细胞器，因此，必须进行分裂，以便每个子寄生虫在细胞分裂期间继承一个顶质体。在这项研究中，我们确定了F-肌动蛋白和一个非常规的肌球蛋白马达，TgMyoF，在这个过程中的新角色。首先，TgMyoF和肌动蛋白的损失导致顶质体囊泡在胞质溶胶中的积累，表明该肌动球蛋白系统在顶质体蛋白运输或细胞器的形态完整性中的作用。第二，活细胞成像显示，在分裂的顶质体是高度动态的，表现出分支，U形和线性的形态，依赖于TgMyoF和肌动蛋白。在运动被TgMyoF耗尽抑制的寄生虫中，顶质体未能与寄生虫中心体结合。因此，这项研究提供了至关重要的新的洞察机制控制顶质体中心体协会，在顶质体分裂周期的一个重要步骤，这确保每个女儿继承一个单一的apicoplast.IMPORTANCEToxoplasma gondii和大多数其他寄生虫在门Apicomplexa包含一个顶质体，非光合质体细胞器所需的脂肪酸，类异戊二烯，铁硫簇，和血红素合成。顶质体功能的扰动导致寄生虫死亡。因此，寄生虫的生存主要取决于两个细胞过程：顶质体分裂，以确保每个子寄生虫继承一个顶质体，并将核编码的蛋白质运输到顶质体。尽管这些过程的重要性，有显着的知识差距方面控制这些过程的分子机制，这是特别真实的核编码顶质体蛋白的运输。这项研究提供了至关重要的新的见解顶质体蛋白质合成和运输的顶质体的时间。此外，这项研究表明，顶质体中心体协会，在顶质体分裂周期的关键步骤，是由肌动球蛋白细胞骨架控制。
Toxoplasma gondiicontains an essential plastid organelle called the apicoplast that is necessary for fatty acid, isoprenoid, and heme synthesis. Perturbations affecting apicoplast function or inheritance lead to parasite death. The apicoplast is a single copy organelle and, therefore, must be divided so that each daughter parasite inherits an apicoplast during cell division. In this study, we identify new roles for F-actin and an unconventional myosin motor, TgMyoF, in this process. First, loss of TgMyoF and actin lead to an accumulation of apicoplast vesicles in the cytosol indicating a role for this actomyosin system in apicoplast protein trafficking or morphological integrity of the organelle. Second, live cell imaging reveals that during division the apicoplast is highly dynamic, exhibiting branched, U-shaped and linear morphologies that are dependent on TgMyoF and actin. In parasites where movement was inhibited by the depletion of TgMyoF, the apicoplast fails to associate with the parasite centrosomes. Thus, this study provides crucial new insight into mechanisms controlling apicoplast-centrosome association, a vital step in the apicoplast division cycle, which ensures that each daughter inherits a single apicoplast.IMPORTANCEToxoplasma gondiiand most other parasites in the phylum Apicomplexa contain an apicoplast, a non-photosynthetic plastid organelle required for fatty acid, isoprenoid, iron-sulfur cluster, and heme synthesis. Perturbation of apicoplast function results in parasite death. Thus, parasite survival critically depends on two cellular processes: apicoplast division to ensure every daughter parasite inherits a single apicoplast, and trafficking of nuclear encoded proteins to the apicoplast. Despite the importance of these processes, there are significant knowledge gaps in regards to the molecular mechanisms which control these processes; this is particularly true for trafficking of nuclear-encoded apicoplast proteins. This study provides crucial new insight into the timing of apicoplast protein synthesis and trafficking to the apicoplast. In addition, this study demonstrates how apicoplast-centrosome association, a key step in the apicoplast division cycle, is controlled by the actomyosin cytoskeleton.