PDF(Pubmed)
Abstract：
The Drosophila eye develops from the larval eye disc, a flattened vesicle comprised of continuous retinal and peripodial epithelia (PE). The PE is an epithelium that plays a supporting role in retinal neurogenesis, but gives rise to cuticle in the adult. We report here that the PE is also necessary to preserve the morphology of the retinal epithelium. Depletion of the adherens junction (AJ) components β-Catenin (β-Cat), DE-Cadherin or α-Catenin from the PE leads to altered disc morphology, characterized by retinal displacement (RDis); so too does loss of the Ajuba protein Jub, an AJ-associated regulator of the transcriptional coactivator Yorkie (Yki). Restoring AJs or overexpressing Yki in β-Cat deficient PE results in suppression of RDis. Additional suppressors of AJ-dependent RDis include knockdown of Rho kinase (Rok) and Dystrophin (Dys). Furthermore, knockdown of βPS integrin (Mys) from the PE results in RDis, while overexpression of Mys can suppress RDis induced by the loss of β-Cat. We thus propose that AJ-Jub-Yki signaling in PE cells regulates PE cell contractile properties and/or attachment to the extracellular matrix to promote normal eye disc morphology.
摘要：
果蝇眼是从幼虫眼盘发育而来的,由连续的视网膜和周围上皮（PE）组成的扁平囊泡。PE是在视网膜神经发生中起辅助作用的上皮,但在成人中会产生角质层。我们在这里报道，PE对于保持视网膜上皮的形态也是必要的。粘附连接（AJ）成分β-连环蛋白（β-Cat）的消耗，PE的DE-Cadherin或α-Catenin导致椎间盘形态改变，以视网膜位移（RDis）为特征；Ajuba蛋白Jub的丢失也是如此，转录共激活因子Yorkie（Yki）的AJ相关调节因子。在β-Cat缺陷型PE中恢复AJ或过表达Yki导致RDis的抑制。AJ依赖性RDis的其他抑制剂包括Rho激酶(Rok)和肌营养不良蛋白(Dys)的敲减。此外，从PE中敲低βPS整合素(Mys)导致RDis，而Mys的过表达可以抑制β-Cat缺失诱导的RDis。因此，我们建议PE细胞中的AJ-Jub-Yki信号传导调节PE细胞收缩特性和/或与细胞外基质的附着以促进正常的眼盘形态。
