研究生: |
何育慧 Yu-Huei Ho |
---|---|
論文名稱: |
黏著性分子Echinoid在平面細胞極性所扮演的角色探討 The role of adhesion molecule Echinoid in planar cell polarity |
指導教授: |
徐瑞洲
Jui-Chou Hsu |
口試委員: | |
學位類別: |
碩士 Master |
系所名稱: |
生命科學暨醫學院 - 分子醫學研究所 Institute of Molecular Medicine |
論文出版年: | 2006 |
畢業學年度: | 94 |
語文別: | 英文 |
論文頁數: | 37 |
中文關鍵詞: | 平面極性 |
外文關鍵詞: | planar cell polarity, Ed |
相關次數: | 點閱:2 下載:0 |
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平面細胞極性(簡稱PCP)是一種常見於多細胞表皮組織的特性,其極性對稱軸垂直於頂底軸。不論在果蠅或是脊椎動物,平面細胞極性廣泛表現在很多不同的細胞類型和身體組織上。平面細胞極性擁有一群高度保留的蛋白質,稱之為核心平面細胞極性蛋白,包含有frizzled (fz)、disheveled (dsh)、flamingo (Fmi)/ starry night (stan)、prickle (pk)、strabismus (stbm)/ Van Gogb(Vang)和diego (dgo)等,藉由核心蛋白的不對稱分佈來提供正確的平面細胞極性訊息。平面細胞極性在果蠅複眼的功能是在發育過程中協調位處背腹部的小眼各自旋轉90度,使其依背腹軸形成鏡像對稱,而要使此過程有正確的旋轉角度就要有正確的R3/R4細胞命運的選擇,平面細胞極性的作用正是調控R3/R4細胞的選擇。
Echinoid (Ed) 是一個具有免疫球蛋白區域(immunoglobulin domain)的細胞黏著分子,可在眼睛發育過程中負調控EGFR訊息,也可和Notch訊息合作影響感覺性剛毛的發育。此外,也發現Ed是Adherens Junctions (AJs)的一員,可和DE-cadherin共同調控細胞黏著。
在此篇論文,我們發現在ed突變的情況下,Fmi在小眼間細胞的表現量會上升,並提高至與小眼細胞的表現量相仿,而且ed突變的成蟲複眼會變的不平整且具有錯誤轉向的小眼存在。此外, Fmi在小眼間細胞的錯位表現會使小眼產生錯誤轉向的現象,此現象就類似於ed突變的情形,因此,這些結果顯示Fmi在小眼間細胞的調控和在小眼細胞是同等重要的,而ed可能在這過程中扮演著調控的角色。
Planar cell polarity (PCP) is a common feature of many multicellular epithelia and is perpendicular to their apical/basal axis. PCP is manifest in several different body regions and cell types of vertebrates and Drosophila. The conserved PCP proteins called core PCP include frizzled (fz), disheveled (dsh), flamingo (Fmi)/ starry night (stan), prickle (pk), strabismus (stbm)/ Van Gogb(Vang), and diego (dgo). The asymmetric distribution of core PCP provides the correct cues for PCP. In Drsophila eye, PCP is evident in the coordinated orientation of ommatidia that rotate 90° in opposite directions in the dorsal and ventral halves of the eye during eye development. The key point for ommatidia to rotate correctly is the decision of R3/R4 fate that is controlled by PCP.
Echinoid (Ed) is an immunoglobulin (Ig) domain-containing CAMs. Ed negatively regulates EGF receptor signaling pathway during eye development and cooperates with Notch pathway during sensory bristle development. Moreover, we identified that Ed is a component of Adherens Junctions (AJs) that cooperates with DE-cadherin to mediate cell adhesion.
In this report, we show that when ed is mutated, the expression level of Fmi in interommatidia cells is increased and similar to that in ommatidia cells. Furthermore, adult ed mutation eye shows rough phenotype and misrotated ommatidia. Misexpressing Fmi in eye discs also causes Fmi to be increased mainly in interommatidia cells and leads to misrotated ommatidia, similar to the phenotype in ed mutant eye. These results suggest that the regulation of Fmi in interommatidia cells is as important as that in ommatidia cells, and ed may play such a regulation role in this process.
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