The Drosophila follicle cells as a model for analysis of steroid hormone in regulation of E-cadherin dynamics

• Main Authors: Hui-HuiHsu, 許惠惠
• Other Authors: Chuen-Chuen Jang
• Format: Others
• Language: en_US
• Published: 2014
• Online Access: http://ndltd.ncl.edu.tw/handle/jsq6t9

碩士 === 國立成功大學 === 生物科技研究所 === 102 === In animal development, E-cadherin is required for epithelial to change shapes and patterns. Our lab is interested in E-cadherin dynamics during morphogenesis, so we use Drosophila border cells as a model to study E-cadherin in cell migration. Upon detaching of border cells, E-cadherin enriches at the leading edge. During migration, E-cadherin remains accumulated at interfaces of border cells, but is down-regulated in border/nurse cell junctions. Previous study identified the role of ecdysone to regulate E-cadherin dynamics. To test this hypothesis, we increased the level of ecdysone signaling, which caused E-cadherin lost and scattered morphology in border cells. By contrast, decrease of ecdysone signaling resulted in overall increase in E-cadherin. Previous researches show endocytosis regulates E-cadherin dynamics during morphogenesis thus we further test whether ecdysone signaling affect the distributions of endosomal markers. Rab7::GFP, a marker for late endosomes, mainly express at the edge of border cells whereas E-cadherin is more dynamic. But, Rab7::GFP was increased in whole cluster while ecdysone signaling was overexpressed. Suppression of ecdysone signaling caused sustained expression of Rab7::GFP at leading edge, which was not observed in wild type border cells. Taken together, we propose that ecdysone signaling may govern the distributions of E-cadherin in border cell migration through Rab7 mediated endocytosis.