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研究生:廖淑如
研究生(外文):Shu-Ju Liao
論文名稱:gooseberry參與果蠅胚胎背部表皮細胞的閉鎖
論文名稱(外文):Role of gooseberry during dorsal closure in Drosophila development
指導教授:徐瑞洲
指導教授(外文):Jui-Chou Hsu
學位類別:碩士
校院名稱:國立清華大學
系所名稱:生命科學系
學門:生命科學學門
學類:生物學類
論文種類:學術論文
論文出版年:2002
畢業學年度:90
語文別:中文
論文頁數:56
中文關鍵詞:背部表皮細胞的閉鎖果蠅JNK訊號傳遞背板閉鎖
外文關鍵詞:dorsal closureDrosophilagooseberryJNK pathwaythorax closure
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gooseberry(gsb,即為已知的gooseberry-distal,gsb-d)是我們利用DER的持續活化株(ElpB1)篩選P line stock突變株,找到的一個基因,經由進一步的遺傳實驗推測,其為DER訊號傳遞的一個負性調控因子。已知gsb為segment polarity gene亦為核內的轉錄因子,當我們觀察gsb突變株及大量表現Gsb的果蠅胚胎時,發現其皆會造成果蠅胚胎背部表皮細胞閉鎖不全;不同的是,在gsb突變株會有大量phosphotyrosine 聚集在adherens junctions,而在大量表現Gsb的胚胎中,並不會有phosphotyrosine聚集,而是會使LE細胞在stage 13以後不往背腹軸拉長,反而往前後軸的方向拉長。此外,大量表現Gsb在成蠅背板,則是會造成果蠅背板閉鎖不全。已知參與果蠅背部表皮細胞閉鎖及背板閉鎖的主要訊號傳遞為D.melanogaster Jun-N-terminal kinase(DJNK)。我們發現在gsb突變的果蠅中會使pucE69(puc的enhancer trap line)增加puc的表現量,從LE細胞往腹部延伸數排的表皮細胞,而在大量表現Gsb的果蠅胚胎中,則會有puc在LE細胞表現量減少的情形。實驗結果顯示,gsb發生突變時,會促使DJNK訊號傳遞的活化,而在大量表現Gsb時,則是會抑制DJNK訊號傳遞的活化。因此,我們推測gsb亦為DJNK訊號傳遞的一個負性調控因子。總而言之,gsb不僅在胚胎早期調控神經母細胞及腹部表皮細胞的分化、發育,亦會經由抑制DJNK訊號傳遞,進而影響胚胎背部表皮細胞的閉鎖,此外,在幼蟲時期亦參與複眼發育,及蛹期成蠅背板閉鎖的調控。

To identify genes that modulate DER signaling in eye development, we undertook a genetic modifier screen in P line stock. gooseberry ( also know as gooseberry-distal, gsb-d ) is one of the four genes identified in this screen and defines a negative regulator of the DER signal pathway. We show that gsb mutations result in the failure of dorsal closure as the embryo exhibits a hole in the dorsal cuticle. Although ectopic expression of gsb has the similar cuticle phenotype as gsb mutants, the leading edge cells never elongate along the DV axis during stage 13; instead they stretch along the AP axis. Furthermore, overexpression of UAS-Gsb with pnr-GAL4 and eq-GAL4 induces a thorax cleft. The D.melanogaster Jun- N-terminal kinase ( DJNK ) signal transduction pathway, also know as stress-activated MAP kinases ( SAPK ), represent a third group of MAPK. In Drosophila, the JNK pathway is best known for its role in dorsal closure. In gsb mutant embryo, we observed the expansion of pucE69 enhancer trap expression into several rows of cells adjacent to the leading edge. In addition, we also found ectopic P-Tyr staining in lateral cells. In contrast, ectopic expression of gsb leads to a decrease in the expression of pucE69 in leading edge cells. Taken together our data indicate that gsb mutations result in the hyperactivation of DJNK signal, and overexpression of gsb result in downregulation of DJNK signal. Therefore, gsb may also be a negative regulator of the DJNK signal pathway during dorsal closure.

序 I
中文摘要 1
英文摘要 2
緒論 3
材料與方法 9
結果 15
討論 23
參考文獻 28
圖表附錄 35

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