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首页> 外文期刊>Cilia >Basal body positioning and anchoring in the multiciliated cell Paramecium tetraurelia : roles of OFD1 and VFL3
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Basal body positioning and anchoring in the multiciliated cell Paramecium tetraurelia : roles of OFD1 and VFL3

机译：基础体的定位和锚定在多纤毛细胞草履虫：OFD1和VFL3的作用

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Background The development of a ciliary axoneme requires the correct docking of the basal body at cytoplasmic vesicles or plasma membrane. In the multiciliated cell Paramecium, three conserved proteins, FOR20, Centrin 2, and Centrin 3 participate in this process, FOR20 and Centrin 2 being involved in the assembly of the transition zone. We investigated the function of two other evolutionary conserved proteins, OFD1 and VFL3, likely involved in this process. Results In Paramecium tetraurelia , a single gene encodes OFD1, while four genes encode four isoforms of VFL3, grouped into two families, VFL3-A and VFL3-B. Depletion of OFD1 and the sole VFL3-A family impairs basal body docking. Loss of OFD1 yields a defective assembly of the basal body distal part. Like FOR20, OFD1 is recruited early during basal body assembly and localizes at the transition zone between axoneme and membrane at the level of the microtubule doublets. While the recruitment of OFD1 and Centrin 2 proceed independently, the localizations of OFD1 and FOR20 at the basal body are interdependent. In contrast, in VFL3-A depleted cells, the unanchored basal bodies harbor a fully organized distal part but display an abnormal distribution of their associated rootlets which mark their rotational asymmetry. VFL3-A, which is required for the recruitment of Centrin 3, is transiently present near the basal bodies at an early step of their duplication. VFL3-A localizes at the junction between the striated rootlet and the basal body. Conclusion Our results demonstrate the conserved role of OFD1 in the anchoring mechanisms of motile cilia and establish its relations with FOR20 and Centrin 2. They support the hypothesis of its association with microtubule doublets. They suggest that the primary defect of VFL3 depletion is a loss of the rotational asymmetry of the basal body which specifies the sites of assembly of the appendages which guide the movement of basal bodies toward the cell surface. The localization of VFL3 outside of the basal body suggests that extrinsic factors could control this asymmetry.
机译：背景技术睫状轴突的发展需要将基体正确地对接在细胞质囊泡或质膜上。在多纤毛细胞草履虫中，三种保守的蛋白质，FOR20，Centrin 2和Centrin 3参与了此过程，FOR20和Centrin 2参与了过渡区的组装。我们调查了可能参与此过程的其他两个进化保守蛋白OFD1和VFL3的功能。结果在草履虫中，一个基因编码OFD1，而四个基因编码VFL3的四个同工型，分为两个家族，VFL3-A和VFL3-B。 OFD1和唯一的VFL3-A家族的枯竭削弱了基础身体的对接。 OFD1的丢失会导致基体远端部分的组装不良。像FOR20一样，OFD1在基体组装过程中被早期募集，并定位在轴突和膜之间的过渡区的微管双峰水平。尽管OFD1和Centrin 2的募集独立进行，但OFD1和FOR20在基体的定位是相互依赖的。相比之下，在VFL3-A耗尽的细胞中，未锚定的基体具有完整组织的远端部分，但显示出其相关的小根的异常分布，这标志着它们的旋转不对称。募集Centrin 3所需的VFL3-A在复制的早期即刻出现在基体附近。 VFL3-A位于条纹状小根与基体之间的连接处。结论我们的结果证明了OFD1在能动纤毛的锚定机制中的保守作用，并建立了它与FOR20和Centrin 2的关系。它们支持其与微管双联体相关的假说。他们认为，VFL3耗竭的主要缺陷是失去了基体的旋转不对称性，后者指定了引导基体向细胞表面运动的附肢的装配部位。 VFL3在基体外部的定位表明，外在因素可以控制这种不对称性。

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