Zartman Jeremiah J, Yakoby Nir, Bristow Christopher A, Zhou Xiaofeng, Schlichting Karin, Dahmann Christian, Shvartsman Stanislav Y
Lewis Sigler Institute and Department of Chemical Engineering, Carl Icahn Laboratory, Princeton University, Princeton, NJ 08544, USA.
Dev Biol. 2008 Oct 15;322(2):289-301. doi: 10.1016/j.ydbio.2008.07.027. Epub 2008 Jul 30.
Drosophila egg development is an established model for studying epithelial patterning and morphogenesis, but the connection between signaling pathways and egg morphology is still incompletely understood. We have identified a non-classical cadherin, Cad74A, as a putative adhesion gene that bridges epithelial patterning and morphogenesis in the follicle cells. Starting in mid-oogenesis, Cad74A is expressed in the follicle cells that contact the oocyte, including the border cells and most of the columnar follicle cells. However, Cad74A is repressed in two dorsolateral patches of follicle cells, which participate in the formation of tubular respiratory appendages. We show genetically that Cad74A is downstream of the EGFR and BMP signaling pathways and is repressed by the Zn-finger transcription factor Broad. The correlation of Cad74A repression in the cells that bend out of the plane of the follicular epithelium is preserved across Drosophila species and mutant backgrounds exhibiting a range of eggshell phenotypes. Complete removal of Cad74A from the follicle cells causes defects in dorsal appendage formation. Ectopic expression of Cad74A in the roof cells results in shortened, flattened appendages due to the hindered migration of the roof cells. Based on these results, we propose that Cad74A is part of the adhesive machinery that enables robust dorsal appendage formation, and as such provides a link between the patterning of the follicle cells and eggshell morphogenesis.
果蝇卵子发育是研究上皮细胞图案形成和形态发生的一个成熟模型,但信号通路与卵子形态之间的联系仍未完全了解。我们已鉴定出一种非经典钙黏蛋白Cad74A,它是一种假定的黏附基因,在卵泡细胞中连接上皮细胞图案形成和形态发生。从卵子发生中期开始,Cad74A在与卵母细胞接触的卵泡细胞中表达,包括边界细胞和大多数柱状卵泡细胞。然而,Cad74A在卵泡细胞的两个背外侧区域受到抑制,这些区域参与管状呼吸附属物的形成。我们通过遗传学方法表明,Cad74A位于表皮生长因子受体(EGFR)和骨形态发生蛋白(BMP)信号通路的下游,并受到锌指转录因子Broad的抑制。在表现出一系列卵壳表型的果蝇物种和突变背景中,Cad74A在从卵泡上皮平面弯曲出来的细胞中的抑制相关性得以保留。从卵泡细胞中完全去除Cad74A会导致背侧附属物形成缺陷。在顶部细胞中异位表达Cad74A会导致附属物缩短、变平,这是由于顶部细胞迁移受阻所致。基于这些结果,我们提出Cad74A是黏附机制的一部分,它能够实现强大的背侧附属物形成,因此在卵泡细胞图案形成和卵壳形态发生之间提供了一个联系。