Differential expression of the adhesion molecule Echinoid drives epithelial morphogenesis in Drosophila
Differential expression of the adhesion molecule Echinoid drives epithelial morphogenesis in Drosophila
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DOI：
10.1242/dev.02492
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发表时间：
2006-08-15
期刊：
影响因子：
4.6
通讯作者：
Nilson, Laura A.
中科院分区：
文献类型：
--
作者：
Laplante, Caroline;Nilson, Laura A.
上皮细胞形态发生需要细胞运动和细胞形态变化与肌动蛋白细胞骨架的调节相协调。我们发现棘球蛋白(ED)，一种含有免疫球蛋白结构域的细胞黏附分子，在果蝇卵巢卵泡上皮和胚胎上皮形态发生所需的收缩肌球蛋白缆线的产生中发挥作用。对ed突变型毛囊细胞克隆的分析表明，野生型和ed突变型细胞的并列足以触发肌动球蛋白电缆的形成。此外，在野生型卵巢和胚胎中，特定的上皮域缺乏可检测到的ED，因此在有和没有ED的细胞之间建立了内源性界面；这些界面表现出与ed突变克隆产生的异位ED表达边界相同的收缩特征。在卵巢中，这样的界面位于背部附属物原基的两种细胞类型之间。在胚胎中，在羊膜背部闭合时，ED从羊膜中消失，产生与外侧表皮交界处的ED表达边界，该边界与该交界处存在的肌动球蛋白缆线相一致。在这两种情况下，ed突变的上皮细胞都表现出这种收缩结构的丧失和随后的形态发生缺陷。我们认为，ED表达边界细胞骨架的局部调节可能代表了促进上皮形态发生的一般机制。
Epithelial morphogenesis requires cell movements and cell shape changes coordinated by modulation of the actin cytoskeleton. We identify a role for Echinoid (Ed), an immunoglobulin domain-containing cell-adhesion molecule, in the generation of a contractile actomyosin cable required for epithelial morphogenesis in both the Drosophila ovarian follicular epithelium and embryo. Analysis of ed mutant follicle cell clones indicates that the juxtaposition of wild-type and ed mutant cells is sufficient to trigger actomyosin cable formation. Moreover, in wild-type ovaries and embryos, specific epithelial domains lack detectable Ed, thus creating endogenous interfaces between cells with and without Ed; these interfaces display the same contractile characteristics as the ectopic Ed expression borders generated by ed mutant clones. In the ovary, such an interface lies between the two cell types of the dorsal appendage primordia. In the embryo, Ed is absent from the amnioserosa during dorsal closure, generating an Ed expression border with the lateral epidermis that coincides with the actomyosin cable present at this interface. In both cases, ed mutant epithelia exhibit loss of this contractile structure and subsequent defects in morphogenesis. We propose that local modulation of the cytoskeleton at Ed expression borders may represent a general mechanism for promoting epithelial morphogenesis.