Diamond controls epithelial polarity through the dynactin-dynein complex.

IF 3.6 3区生物学 Q3 CELL BIOLOGY

Traffic Pub Date : 2023-12-01 Epub Date: 2023-08-29 DOI:10.1111/tra.12917

Hang Zhao, Lin Shi, Zhengran Li, Ruiyan Kong, Lemei Jia, Shan Lu, Jian-Hua Wang, Meng-Qiu Dong, Xuan Guo, Zhouhua Li

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Abstract

Epithelial polarity is critical for proper functions of epithelial tissues, tumorigenesis, and metastasis. The evolutionarily conserved transmembrane protein Crumbs (Crb) is a key regulator of epithelial polarity. Both Crb protein and its transcripts are apically localized in epithelial cells. However, it remains not fully understood how they are targeted to the apical domain. Here, using Drosophila ovarian follicular epithelia as a model, we show that epithelial polarity is lost and Crb protein is absent in the apical domain in follicular cells (FCs) in the absence of Diamond (Dind). Interestingly, Dind is found to associate with different components of the dynactin-dynein complex through co-IP-MS analysis. Dind stabilizes dynactin and depletion of dynactin results in almost identical defects as those observed in dind-defective FCs. Finally, both Dind and dynactin are also required for the apical localization of crb transcripts in FCs. Thus our data illustrate that Dind functions through dynactin/dynein-mediated transport of both Crb protein and its transcripts to the apical domain to control epithelial apico-basal (A/B) polarity.

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金刚石通过动力蛋白-动力蛋白复合物控制上皮极性。

上皮极性对上皮组织的正常功能、肿瘤发生和转移至关重要。进化上保守的跨膜蛋白碎屑(Crb)是上皮极性的关键调节因子。Crb蛋白及其转录本均位于上皮细胞的顶端。然而，目前还不完全清楚它们是如何靶向于顶域的。在这里，我们以果蝇卵巢滤泡上皮为模型，发现在缺少金刚石(Dind)的情况下，滤泡细胞(FCs)的上皮极性丢失，Crb蛋白在顶端结构域缺失。有趣的是，通过co-IP-MS分析，发现Dind与动力蛋白复合物的不同组分相关联。Dind稳定了动力蛋白，而动力蛋白的缺失导致的缺陷几乎与Dind缺陷fc中观察到的缺陷相同。最后，Dind和dynactin对于FCs中crb转录本的顶端定位也是必需的。因此，我们的数据表明，Dind通过动力蛋白/动力蛋白介导的Crb蛋白及其转录物的转运到顶端结构域来控制上皮的顶基(A/B)极性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Traffic 生物-细胞生物学

CiteScore

8.10

自引率

2.20%

发文量

审稿时长

2 months

期刊介绍： Traffic encourages and facilitates the publication of papers in any field relating to intracellular transport in health and disease. Traffic papers span disciplines such as developmental biology, neuroscience, innate and adaptive immunity, epithelial cell biology, intracellular pathogens and host-pathogen interactions, among others using any eukaryotic model system. Areas of particular interest include protein, nucleic acid and lipid traffic, molecular motors, intracellular pathogens, intracellular proteolysis, nuclear import and export, cytokinesis and the cell cycle, the interface between signaling and trafficking or localization, protein translocation, the cell biology of adaptive an innate immunity, organelle biogenesis, metabolism, cell polarity and organization, and organelle movement. All aspects of the structural, molecular biology, biochemistry, genetics, morphology, intracellular signaling and relationship to hereditary or infectious diseases will be covered. Manuscripts must provide a clear conceptual or mechanistic advance. The editors will reject papers that require major changes, including addition of significant experimental data or other significant revision. Traffic will consider manuscripts of any length, but encourages authors to limit their papers to 16 typeset pages or less.