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A Novel Actin-Related Protein Is Associated with Daughter Cell Formation in Toxoplasma gondii

机译:一种新型肌动蛋白相关蛋白与弓形虫子细胞形成有关

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Cell division in Toxoplasma gondii occurs by an unusual budding mechanism termed endodyogeny, during which twin daughters are formed within the body of the mother cell. Cytokinesis begins with the coordinated assembly of the inner membrane complex (IMC), which surrounds the growing daughter cells. The IMC is compiled of both flattened membrane cisternae and subpellicular filaments composed of articulin-like proteins attached to underlying singlet microtubules. While proteins that comprise the elongating IMC have been described, little is known about its initial formation. Using Toxoplasma as a model system, we demonstrate that actin-like protein 1 (ALP1) is partially redistributed to the IMC at early stages in its formation. Immunoelectron microscopy localized ALP1 to a discrete region of the nuclear envelope, on transport vesicles, and on the nascent IMC of the daughter cells prior to the arrival of proteins such as IMC-1. The overexpression of ALP1 under the control of a strong constitutive promoter disrupted the formation of the daughter cell IMC, leading to delayed growth and defects in nuclear and apicoplast segregation. Collectively, these data suggest that ALP1 participates in the formation of daughter cell membranes during cell division in apicomplexan parasites.
机译:弓形虫的细胞分裂是通过一种异常的萌发机制发生的,该机制称为内生性,在此过程中,在母细胞体内形成了双胞胎女儿。细胞分裂始于内膜复合物(IMC)的协调装配,该膜围绕着正在生长的子细胞。 IMC由平坦的膜水箱和由附着在下面的单线态微管上的青霉素样蛋白组成的亚膜细丝构成。尽管已经描述了包含延伸IMC的蛋白质,但对其初始形成知之甚少。使用弓形虫作为模型系统,我们证明了肌动蛋白样蛋白1(ALP1)在其形成的早期阶段已部分重新分配给IMC。免疫电子显微镜将ALP1定位于核膜的离散区域,转运囊泡以及子细胞初生的IMC上,然后到达蛋白质(如IMC-1)。在强大的组成型启动子的控制下,ALP1的过度表达破坏了子细胞IMC的形成,从而导致了生长延迟以及核和土质分离的缺陷。总的来说,这些数据表明ALP1在apicomplexan寄生虫的细胞分裂过程中参与子细胞膜的形成。

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