Department of Cell and Molecular Biology, Medical Faculty Mannheim, Heidelberg University, D-68167 Mannheim, Germany.
J Cell Biol. 2012 Dec 24;199(7):1131-43. doi: 10.1083/jcb.201207150.
Regulation of epithelial cell shape, for example, changes in relative sizes of apical, basal, and lateral membranes, is a key mechanism driving morphogenesis. However, it is unclear how epithelial cells control the size of their membranes. In the epithelium of the Drosophila melanogaster ovary, cuboidal precursor cells transform into a squamous epithelium through a process that involves lateral membrane shortening coupled to apical membrane extension. In this paper, we report a mutation in the gene Tao, which resulted in the loss of this cuboidal to squamous transition. We show that the inability of Tao mutant cells to shorten their membranes was caused by the accumulation of the cell adhesion molecule Fasciclin 2, the Drosophila N-CAM (neural cell adhesion molecule) homologue. Fasciclin 2 accumulation at the lateral membrane of Tao mutant cells prevented membrane shrinking and thereby inhibited morphogenesis. In wild-type cells, Tao initiated morphogenesis by promoting Fasciclin 2 endocytosis at the lateral membrane. Thus, we identify here a mechanism controlling the morphogenesis of a squamous epithelium.
例如,上皮细胞形状的调节,例如,顶膜、基底膜和侧膜相对大小的变化,是驱动形态发生的关键机制。然而,目前尚不清楚上皮细胞如何控制其膜的大小。在果蝇卵巢的上皮组织中,立方前体细胞通过一个过程转化为鳞状上皮,该过程涉及侧膜缩短与顶膜延伸相结合。在本文中,我们报告了 Tao 基因的一个突变,导致这种立方到鳞状的转变丧失。我们表明, Tao 突变细胞不能缩短其膜的原因是细胞粘附分子 Fasciclin 2(果蝇 N-CAM 的同源物)的积累。Fasciclin 2 在 Tao 突变细胞的侧膜中的积累阻止了膜的收缩,从而抑制了形态发生。在野生型细胞中,Tao 通过促进侧膜处 Fasciclin 2 的内吞作用来启动形态发生。因此,我们在这里确定了一种控制鳞状上皮形态发生的机制。