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Dynein assembly factor with WD repeat domains 1 (DAW1) is required for the function of motile cilia in the planarian Schmidtea mediterranea.
Development, Growth & Differentiation ( IF 2.5 ) Pub Date : 2020-05-02 , DOI: 10.1111/dgd.12669
Sydney Lynn Lesko 1 , Labib Rouhana 1
Affiliation  

Motile cilia propel directed cell movements and sweep fluids across the surface of tissues. Orthologs of Dynein Assembly Factor with WD Repeat Domains 1 (DAW1) support normal ciliary beating by enhancing delivery of dynein complexes to axonemal microtubules. DAW1 mutations in vertebrates result in multiple developmental abnormalities and early or prenatal lethality, complicating functional assessment of DAW1 in adult structures. Planarian flatworms maintain cellular homeostasis and regenerate through differentiation of adult pluripotent stem cells, and systemic RNA‐interference (RNAi) can be induced to analyze gene function at any point after birth. A single ortholog of DAW1 was identified in the genome of the planarian Schmidtea mediterranea (Smeddaw1). Smed‐DAW1 is composed of eight WD repeats, which are 55% identical to the founding member of this protein family (Chlamydomonas reinhardtii ODA16) and 58% identical to human DAW1. Smeddaw1 is expressed in the planarian epidermis, protonephridial excretory system, and testes, all of which contain cells functionally dependent on motile cilia. Smed‐daw1 RNAi resulted in locomotion defects and edema, which are phenotypes characteristic of multiciliated epidermis and protonephridial dysfunction, respectively. Changes in abundance or length of motile cilia were not observed at the onset of phenotypic manifestations upon Smed‐daw1 RNAi, corroborating with studies showing that DAW‐1 loss of function leads to aberrant movement of motile cilia in other organisms, rather than loss of cilia per se. However, extended RNAi treatments did result in shorter epidermal cilia and decreased abundance of ciliated protonephridia, suggesting that Smed‐daw1 is required for homeostatic maintenance of these structures in flatworms.

中文翻译:

具有 WD 重复结构域 1 (DAW1) 的动力蛋白组装因子是地中海涡虫 Schmidtea 中运动纤毛的功能所必需的。

运动纤毛推动定向细胞运动,并在组织表面扫过液体。的直系同源物d yneinssembly因子与W¯¯通过增强微管轴丝动力蛋白复合物的递送d重复结构域1(DAW1)支持正常的纤毛跳动。脊椎动物中的 DAW1 突变导致多种发育异常和早期或产前致死率,使成年结构中 DAW1 的功能评估复杂化。涡虫通过成体多能干细胞的分化来维持细胞稳态和再生,并且可以在出生后的任何时间诱导系统性 RNA 干扰 (RNAi) 来分析基因功能。在地中海涡虫 Schmidtea 的基因组中鉴定出 DAW1 的单一直系同源物( Smed - daw1 )。Smed-DAW1 由 8 个 WD 重复序列组成,与该蛋白质家族的创始成员(莱茵衣藻ODA16)有 55% 的相同性,与人类 DAW1 有 58% 的相同性。Smed - daw1在涡虫表皮、原肾排泄系统和睾丸中表达,所有这些都包含在功能上依赖于运动纤毛的细胞。Smed-daw1 RNAi 导致运动缺陷和水肿,分别是多纤毛表皮和原肾功能障碍的表型特征。在Smed-daw1表型表现开始时未观察到运动纤毛丰度或长度的变化RNAi,证实了研究表明 DAW-1 功能丧失导致其他生物体中运动纤毛的异常运动,而不是纤毛本身的丧失。然而,延长的 RNAi 治疗确实导致表皮纤毛变短和纤毛原肾的丰度减少,这表明Smed-daw1是扁虫中这些结构的稳态维持所必需的。
更新日期:2020-05-02
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