The cooperative roles of two kinetoplastid-specific kinesins in cytokinesis and in maintaining cell morphology in bloodstream trypanosomes.
The cooperative roles of two kinetoplastid-specific kinesins in cytokinesis and in maintaining cell morphology in bloodstream trypanosomes.
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两种动质体特异性驱动蛋白在胞质分裂和维持血流锥虫细胞形态中的协同作用。
DOI：
10.1371/journal.pone.0073869
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Li Z
中科院分区：
文献类型：
--
作者：
Wei Y;Hu H;Lun ZR;Li Z
布氏锥虫是一种单细胞真核生物，也是一种寄生原生动物，其细胞骨架由分布在质膜下的膜下微管束状结构所定义。我们最近发现了两个孤儿Kinesin，TbKIN-C和TbKIN-D，它们合作调节膜下微管胸衣的组织，从而维持布氏毛滴虫原周期形式的细胞形态。在这份报告中，我们描述了TbKIN-C和TbKIN-D在布鲁氏毛滴虫血流形式中的功能，并研究了它们在血流和原循环形式中的功能协作。TbKIN-C和TbKIN-D在体内以血流形式形成紧密的复合体。TbKIN-C在细胞的后端高度富含，而TbKIN-D在细胞周期的各个时期分布于整个细胞体。由于胞质分裂缺陷，血流状态下的TbKIN-C或TbKIN-D的RNAi可抑制细胞增殖并导致细胞死亡。TbKIN-C和TbKIN-D的RNAi也导致基体分离缺陷，但不影响鞭毛和鞭毛附着区(FAZ)丝的合成和分离。TbKIN-C和TbKIN-D的敲除不会破坏膜下微管束带的组织，但会产生具有扩大的鞭毛袋和错位的鞭毛的多核细胞。有趣的是，TbKIN-C的耗尽会导致TbKIN-D的快速降解，同样，TbKIN-C的敲除也会破坏TbKIN-D的稳定性，这表明TbKIN-C/TbKIN-D复合体的形成稳定了两个Kinesin，这是两个Kinesin执行其基本细胞功能所必需的。综上所述，我们的结果证明了这两个动蛋白在血流形态的细胞形态发生和胞质分裂中的重要作用，以及维持这两个动蛋白稳定性所需的异构体复合体的形成。
The cytoskeleton of Trypanosoma brucei, a unicellular eukaryote and a parasitic protozoan, is defined by the subpellicular microtubule corset that is arranged underneath the plasma membrane. We recently identified two orphan kinesins, TbKIN-C and TbKIN-D, that cooperate to regulate the organization of the subpellicular microtubule corset and thereby maintain cell morphology in the procyclic form of T. brucei. In this report, we characterize the function of TbKIN-C and TbKIN-D in the bloodstream form of T. brucei and investigate their functional cooperation in both the bloodstream and procyclic forms. TbKIN-C and TbKIN-D form a tight complex in vivo in the bloodstream form. TbKIN-C is strongly enriched at the posterior tip of the cell, whereas TbKIN-D is distributed throughout the cell body at all cell cycle stages. RNAi of TbKIN-C or TbKIN-D in the bloodstream form inhibits cell proliferation and leads to cell death, due to cytokinesis defects. RNAi of TbKIN-C and TbKIN-D also results in defects in basal body segregation, but does not affect the synthesis and segregation of the flagellum and the flagellum attachment zone (FAZ) filament. Knockdown of TbKIN-C and TbKIN-D does not disrupt the organization of the subpellicular microtubule corset, but produces multinucleated cells with an enlarged flagellar pocket and misplaced flagella. Interestingly, depletion of TbKIN-C results in rapid degradation of TbKIN-D and, similarly, knockdown of TbKIN-C destabilizes TbKIN-D, suggesting that formation of TbKIN-C/TbKIN-D complex stabilizes both kinesins and is required for the two kinesins to execute their essential cellular functions. Altogether, our results demonstrate the essential role of the two kinesins in cell morphogenesis and cytokinesis in the bloodstream form and the requirement of heteromeric complex formation for maintaining the stability of the two kinesins.
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细胞因子和维持锥虫锥虫的细胞形态所必需的动力质体特异性驱动蛋白。
影响因子：
3.6
作者：
Hu L;Hu H;Li Z
通讯作者：
Li Z
影响因子：
11.4
作者：
Kohl, L;Robinson, D;Bastin, P
通讯作者：
Bastin, P
影响因子：
4.8
作者：
Hammarton, TC;Clark, J;Mottram, JC
通讯作者：
Mottram, JC
DOI：
10.1073/pnas.252409199
发表时间：
2002-12-10
影响因子：
11.1
作者：
Kaseda, K;Higuchi, H;Hirose, K
通讯作者：
Hirose, K
影响因子：
4.8
作者：
Li, ZY;Zou, CB;Wang, CC
通讯作者：
Wang, CC