| Abstract | 第6-7页 |
| 中文摘要 | 第8-10页 |
| Abbreviations | 第10-13页 |
| Introduction | 第13-51页 |
| 1 The concept of morphogen | 第13-26页 |
| 1.1 The example of morphogen | 第14-17页 |
| 1.1.1 Examples of morphogen in Drsophila | 第15-16页 |
| 1.1.2 Examples of morphogen in other organisms | 第16-17页 |
| 1.2 Gradient formation and movement | 第17-22页 |
| 1.2.1 Transport Model 1:Free diffusion | 第18-19页 |
| 1.2.2 Transport Model 2:Hindered diffusion | 第19页 |
| 1.2.3 Transport Model 3:Facilitated diffusion and shuttling | 第19-20页 |
| 1.2.4 Transport Model 4: Planar transcytosis | 第20页 |
| 1.2.5 Transport Model 5:Cytonemes | 第20-22页 |
| 1.3 Gradient interpretation | 第22-26页 |
| 1.3.1 The intracellular transduction of gradient signal | 第22-24页 |
| 1.3.2 Morphogen gradient determines cell identity through the level of transcriptionaleffector activated | 第24-25页 |
| 1.3.3 Strategies employed in the regulation of differentially responsive genes | 第25-26页 |
| 2 The specification of border cells in the ovary of Drosophila melanogaster | 第26-41页 |
| 2.1 The overview of oogenesis | 第27-31页 |
| 2.1.1 The germarium | 第27-28页 |
| 2.1.2 The vitellarium | 第28-31页 |
| 2.2 Border cell specification | 第31-41页 |
| 2.2.1 Temporal control mechanisms of migratory border cell | 第31-32页 |
| 2.2.2 The spatial patterning of migratory border cell | 第32-39页 |
| 2.2.3 The integration of temporal and spatial signals in border cell migration | 第39-41页 |
| 3 The SOCS proteins | 第41-48页 |
| 3.1 The structure of SOCS family proteins | 第41-43页 |
| 3.2 The function of SOCS family proteins | 第43-44页 |
| 3.3 The stability and degradation of SOCS family proteins | 第44-45页 |
| 3.4 The roles of SOCS36E in border cell specification of Drosophila | 第45-48页 |
| 4 The Drosophila insulin signaling pathway through Aktl and TORC1 | 第48-51页 |
| 4.1 The cascade of InR/Aktl/TORC1 signaling pathway | 第48-50页 |
| 4.2 The roles of DLnR/DAktl/DTor signaling pathway inDrosophila developmental events | 第50-51页 |
| Chapter 1 Loss of DAkt function in Drosophila anterior follicle cells lead to ectopic border cells following the normal border cell cluster | 第51-58页 |
| Results | 第54-58页 |
| 1.1 Loss of Akt function in anterior follicle cells through mosaic analysis lead to border cellmigration delay | 第54-55页 |
| 1.2 Additional cells located behind normal border cells, which is subsequently demonstratedas border cells, are observed in Akt mosaic clones | 第55-58页 |
| Chapter 2 The phenotype of ectopic border cells in DAkt mosaic clones is attributed to the increased activity of STAT by the reduction of SOCS36E protein level | 第58-67页 |
| Results | 第60-67页 |
| 2.1 The enhancement of STAT activity is observed in Akt mutant clones | 第61-62页 |
| 2.2 Egg chamber development in wild type ovary and STAT, Eya and Apt protein expressionpattern in wild type during different stages | 第62-64页 |
| 2.3 The increased expression of Apt and Eya, which are molecules in JAK/STAT signalingpathway, is found in Akt mutant clones | 第64-65页 |
| 2.4 The rising activity of STAT in Akt mutant clones is induced by the reduction of SOCS36Eprotein level | 第65-67页 |
| Chapter 3 The same phenotype is shown in both DInR and DTor mosaic clones suggests that InR/Akt/Tor signaling pathway plays essential roles in border cell specification | 第67-73页 |
| 3.1 Additional border cells are observed in InR and TOR mutant clones | 第68-70页 |
| 3.1.1 InR mosaic clones show similar phenotype to Akt mutant clones indicates InR isupstream of Akt in specifying border cell cluster | 第68页 |
| 3.1.2 Akt kinase optimizes border cell number through TOR | 第68-70页 |
| 3.2 Increased STAT activity is observed both in InR and TOR mutant clones | 第70页 |
| 3.3 The increased protein level of Eya and Apt are also observed in both InR and TOR mutantborder cells | 第70-71页 |
| 3.4 The reduction of SOCS36E protein levels both in InR and TOR mutant clones lead to therising STAT activity | 第71-73页 |
| 3.4.1 Decreased SOCS36E protein level are shown in mutant follicle cells expressingdecreased InR and TOR | 第71-72页 |
| 3.4.2 Colocaliization of increased STAT activity and down regulated SOCS36E in InRand TOR mutant clones are shown | 第72-73页 |
| Chapter 4 The phenotype is verified in downregulated molecules involving Insulin signaling pathway using RNAi knock down technique | 第73-82页 |
| 4.1 Downregulation of TorC1 instead of TORC2 using RNA interference cause ectopic bordercell formation | 第74-77页 |
| 4.2 Downregulation of InR, Akt, and Raptor using RNA interference cause ectopic border cellformation | 第77-79页 |
| 4.3 Less anterior follicle cells are turn to be border cells in downregulated expression of Ptenand Tscl/Tsc2 using RNAi knock down, respectively | 第79-80页 |
| 4.4 Up or down regulation of SOCS36E rescued the phenotype caused by InR/Akt/Raptor orPten/Tscl RNAi | 第80-82页 |
| Chapter 5 InR/Akt/TORCl pathway promotes the protein stability of SOCS36E | 第82-90页 |
| 5.1 Increase of SOCS36E protein level is not resulted from TORC1's translation promotingfunction | 第83-85页 |
| 5.2 The InR/Akt/TORC1 signaling pathway promotes the protein stability | 第85-87页 |
| 5.3 TORC1 interacts with SOCS36E and inhibits its proteasomal degradation | 第87-90页 |
| Discussion | 第90-92页 |
| Materials and Methods | 第92-101页 |
| References | 第101-112页 |
| Acknowledgement | 第112-113页 |
| Publication | 第113-115页 |
