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Primary ciliary dyskinesia relative protein ZMYND10 is involved in regulating ciliary function and intraflagellar transport in Paramecium tetraurelia
European Journal of Protistology ( IF 2.9 ) Pub Date : 2020-11-22 , DOI: 10.1016/j.ejop.2020.125756
Lei Shi , Xiangyu Shen , Yuhao Chi , Yuan Shen

Cilia are highly conserved in most eukaryotes and are regarded as an important organelle for motility and sensation in various species. Cilia are microscopic, hair-like cytoskeletal structures that protrude from the cell surface. The major focus in studies of cilia has been concentrated on the ciliary dysfunction in vertebrates that causes multisymptomatic diseases, which together are referred to as ciliopathies. To date, the understanding of ciliopathies has largely depended on the study of ciliary structure and function in different animal models. Zinc finger MYND-type containing 10 (ZMYND10) is a ciliary protein that was recently found to be mutated in patients with primary ciliary dyskinesia (PCD). In Paramecium tetraurelia, we identified two ZMYND10 genes, arising from a whole-genome duplication. Using RNAi, we found that the depletion of ZMYND10 in P. tetraurelia causes severe ciliary defects, thus provoking swimming dysfunction and lethality. Moreover, we found that the absence of ZMYND10 caused the abnormal localization of the intraflagellar transport (IFT) protein IFT43 along cilia. These results suggest that ZMYND10 is involved in the regulation of ciliary function and IFT, which may contribute to the study of PCD pathogenesis.



中文翻译:

原发性纤毛运动障碍的相对蛋白质ZMYND10参与调节纤毛功能和intraflagellar运输草履虫tetraurelia

纤毛在大多数真核生物中是高度保守的,被认为是各种物种运动和感觉的重要细胞器。纤毛是从细胞表面突出的微观的,像头发一样的细胞骨架结构。纤毛研究的主要重点一直放在引起多症状疾病的脊椎动物的睫状功能障碍上,这些疾病统称为纤毛病。迄今为止,对纤毛病的理解很大程度上取决于对不同动物模型中纤毛结构和功能的研究。含有10个锌指的MYND型(ZMYND10)是一种睫状蛋白,最近被发现在原发性睫状运动障碍(PCD)患者中发生了突变。在草履虫,我们鉴定了两个ZMYND10基因,它们来自全基因组重复。使用RNAi,我们发现ZMYND10的耗尽P. tetraurelia造成严重的纤毛缺陷,从而挑起游泳功能障碍和杀伤力。此外,我们发现ZMYND10的缺失会导致沿纤毛的鞭毛内转运(IFT)蛋白IFT43的异常定位。这些结果表明ZMYND10参与了睫状功能和IFT的调节,可能有助于PCD发病机理的研究。

更新日期:2020-12-03
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