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Polarity and morphogenesis of the eye epithelium requires the adhesion junction associated adaptor protein Traf4

机译:眼上皮的极性和形态发生要求粘附结颈相关的适配器蛋白质TRAF4

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摘要

During development, neuroepithelial progenitors acquire apico-basal polarity and adhere to one another via apically located tight and adherens junction complexes. This polarized neuroepithelium must continue to integrate cells arising through cell divisions and intercalation, and allow for cell movements, at the same time as undergoing morphogenesis. Cell proliferation, migration and intercalation all occur in the morphing embryonic eye. To understand how eye development might depend on dynamic epithelial adhesion, we investigated the function of a known regulator of junctional plasticity, Tumour necrosis factor receptor-associated factor 4 (Traf4). traf4a mRNA is expressed in the developing eye vesicle over the period of optic cup morphogenesis, and Traf4a loss leads to disrupted evagination and elongation of the eye vesicles, and aberrant organization and apico-basal polarity of the eye epithelium. We propose a model whereby Traf4a regulates apical junction plasticity in nascent eye epithelium, allowing for its polarization and morphogenesis.
机译:在开发期间,神经头脑祖的祖细胞率获得APICO-基础极性,并通过顶部位于紧密和粘附的结络合物彼此互相粘附。该偏振的神经沉积钠必须继续整合通过细胞部门和插层产生的细胞,并允许细胞运动,同时经受发生的形态发生。细胞增殖,迁移和插层一切都发生在变形胚胎眼中。要了解眼睛发育如何依赖于动态上皮粘附,我们研究了已知的结塑性调节剂,肿瘤坏死因子受体相关因子4(TRAF4)的功能。在光学杯形态发生的时期,TRAF4A mRNA在显影眼囊肿中表达,并且TRAF4A损失导致眼囊泡的失去和伸长,以及眼上皮的异常组织和APICO-基础极性。我们提出了一种模型,即Traf4a调节新生眼上皮中的顶端结可塑性,从而允许其极化和形态发生。

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